tVNS and Chronic Migraine: What the Evidence Actually Shows | For Clinicians | Neuromodulation for Rehabilitation

Why This Article?

Migraine is the second leading cause of years lived with disability worldwide and the leading cause among women aged 15 to 49. In the UK, roughly 10 million adults live with migraine, and approximately 1 million of these have chronic migraine, defined as 15 or more headache days per month for at least 3 months, with at least 8 of those days meeting criteria for migraine.

Current first-line preventive medications provide only partial benefit for many patients. Topiramate achieves a 50% responder rate of approximately 35 to 45%, but with significant cognitive, mood, and teratogenic side effects. Propranolol and amitriptyline have modest efficacy with their own side effect burdens. Even the newer CGRP monoclonal antibodies, which represent a genuine advance, achieve 50% responder rates of 27 to 61% and are typically only available through the NHS after failure of at least three prior preventive treatments.

Complicating matters further, medication overuse headache (MOH) affects 50 to 80% of chronic migraine patients presenting to specialist headache clinics. Any treatment that can reduce reliance on acute medication has intrinsic value in this population.

This creates a genuine need for safe, well-tolerated, home-based approaches that are free from drug interactions and do not contribute to medication overuse. This is the space that transcutaneous vagus nerve stimulation (tVNS) occupies.

Anatomical Concepts distributes the tVNS® system in the UK, and this article provides clinicians with a thorough overview of the evidence for tVNS in migraine. There are numerous wellness devices for vagus nerve stimulation, but only the tVNS® system is a regulated medical device and can substantiate medical claims.

What does the research actually show? Where is the evidence strong, and where are the gaps?

Let me walk you through it.

The Clinical Challenge: Chronic Migraine

Before looking at the solution, it's worth understanding the scale of the problem.

People with chronic migraine experience substantially greater disability than those with episodic migraine. The CaMEO-I study confirmed that chronic migraine is associated with significantly higher rates of depression, anxiety, disability, and healthcare utilisation across multiple countries. In the UK, headaches and migraines account for 5% of all sickness absences.

The European Headache Federation defines resistant migraine as failure of at least three preventive drug categories, and refractory migraine as failure of all available categories. A substantial proportion of patients fall into these categories.

Despite the recent arrival of CGRP-targeted therapies and gepants, many patients with chronic migraine do not achieve satisfactory improvement. OnabotulinumtoxinA (Botox, PREEMPT protocol) achieves a 50% responder rate of approximately 45% at 24 weeks but requires specialist injections every 12 weeks. CGRP monoclonal antibodies are expensive and NICE recommends them only after failure of at least three prior preventive treatments. Non-pharmacological approaches that are safe, well-tolerated, and home-based represent a genuinely important addition to the therapeutic landscape.

Why the Ear? The Anatomy Behind tVNS

If you're going to stimulate the vagus nerve through the skin, you need a reliable access point. The auricular branch of the vagus nerve (ABVN), sometimes called Arnold's nerve, provides exactly that.

The ABVN arises from the superior ganglion of the vagus nerve within the jugular foramen, traverses a small bony canal in the petrous bone, and emerges from the tympanomastoid fissure to innervate portions of the external ear.

The critical issue is where on the ear you stimulate. The cadaver dissection study by Peuker and Filler (2002) established that the cymba conchae has 100% vagal innervation, compared with approximately 45% at the tragus. The landmark fMRI study by Frangos et al. (2015) confirmed in living humans that cymba conchae stimulation produces significant activation of the nucleus tractus solitarius (NTS), locus coeruleus, dorsal raphe, amygdala, and nucleus accumbens.

Critically, migraine-specific fMRI studies have confirmed this pathway is relevant. Zhang et al. (2019) demonstrated that taVNS at the cymba conchae modulates activity in brainstem nuclei (locus coeruleus, raphe nuclei, parabrachial nucleus, NTS) in migraine patients specifically, and that changes in locus coeruleus connectivity with the somatosensory cortex correlated with migraine attack frequency. Chen et al. (2023) showed that repeated taVNS modulates functional connectivity of key brainstem regions in migraine patients, with NTS connectivity changes associated with clinical improvement.

This anatomical precision matters enormously: stimulation at the wrong site simply does not activate the brainstem pathways that drive the therapeutic effect.

How Does tVNS Work in Migraine?

The mechanism by which tVNS modulates migraine pathophysiology is multifactorial and well characterised, engaging pathways that are directly relevant to how migraine attacks are initiated, propagated, and sustained.

The Trigeminovagal Connection

The trigeminovascular system is the primary neural substrate of migraine. Activation of trigeminal afferents innervating the meninges leads to release of CGRP (calcitonin gene-related peptide) and activation of second-order neurons in the trigeminocervical complex (TCC). The vagus nerve and trigeminal nerve converge in the brainstem: the NTS has direct and indirect connections with the trigeminal nucleus caudalis and the broader TCC. This "trigeminovagal connection" is the foundation for how vagal stimulation modulates migraine.

Modulation of the Trigeminocervical Complex

Animal studies provide direct evidence that VNS suppresses nociceptive activation of trigeminocervical neurons. Oshinsky et al. (2014) demonstrated dose-dependent inhibition of dural-vascular trigeminal neurons in rat models. The mechanism involves suppression of glutamate release and microglial activation in the TCC while enhancing GABA release, fundamentally restoring dysfunctional balance in the trigeminal pain processing system.

Effects on CGRP

CGRP is the most established molecular mediator of migraine. It is the target of the CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) and gepants (rimegepant, atogepant). VNS has been shown to reduce CGRP expression in trigeminal ganglia in animal models, with transcutaneous VNS demonstrating attenuation of CGRP expression triggered by cortical spreading depression (Chen et al., 2022). This provides a mechanistic link between vagal stimulation and the same neuropeptide pathway targeted by the newest pharmacological treatments.

Cortical Spreading Depression

Cortical spreading depression (CSD) is a slowly propagating wave of neuronal depolarisation across the cortex, thought to underlie migraine aura and to trigger the trigeminovascular cascade. VNS inhibits CSD through central mechanisms:

Chen et al. (2016) demonstrated that both invasive VNS and transcutaneous VNS inhibit CSD frequency and elevate electrical thresholds for CSD initiation, to the same degree
Chen et al. (2020) established that VNS inhibits CSD exclusively through central mechanisms via the NTS
Liu et al. (2024) identified a glutamate-dependent TrkB activation mechanism in the NTS
nVNS suppresses CSD susceptibility in an intensity-dependent manner

This CSD-inhibiting property is particularly relevant for migraine with aura, and may explain the clinical finding that patients with migraine with aura respond preferentially to nVNS.

Serotonergic and Noradrenergic Modulation

NTS projections to the dorsal raphe nuclei provide a direct pathway for serotonergic modulation. Serotonin is central to migraine pathophysiology: low serotonergic tone is associated with migraine susceptibility, and triptans act as 5-HT1B/1D receptor agonists. VNS increases serotonin release from the raphe nuclei, enhancing descending inhibition of trigeminal nociception.

The locus coeruleus norepinephrine system is also directly engaged. Zhang et al. (2019) demonstrated using fMRI that taVNS at 1 Hz modulates locus coeruleus activity in migraine patients and increases its connectivity with the somatosensory cortex. This increased connectivity was significantly negatively correlated with migraine attack frequency.

Anti-Inflammatory Effects

The cholinergic anti-inflammatory pathway is engaged by VNS, suppressing pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6). nVNS has been shown to suppress CSD-induced neuroinflammation, reducing cortical COX-2 expression and c-Fos expression in the trigeminal nucleus caudalis. This is directly relevant to the neuroinflammatory component of migraine pathophysiology.

KEY POINT: The mechanisms of tVNS in migraine are multi-layered and converging: direct inhibition of trigeminocervical nociceptive neurons, suppression of cortical spreading depression, reduction of CGRP expression, enhancement of descending serotonergic and noradrenergic pain inhibition, and anti-inflammatory effects. This mechanistic breadth distinguishes tVNS from single-target pharmacological approaches and provides a rationale for its use across both acute and preventive indications.

Stimulation Parameters: A Key Difference from Epilepsy

Clinical trials in migraine have revealed an important and somewhat surprising finding about optimal stimulation parameters.

Auricular tVNS Parameters in Migraine

Parameter	Chronic Migraine (Straube 2015)	fMRI Studies in Migraine
Frequency	1 Hz (outperformed 25 Hz)	1 Hz
Pulse width	250 µs	200 µs
Intensity	Maximum tolerated, sub-pain	1.5 to 5 mA
Duty cycle	Continuous	Continuous
Daily duration	4 hours	30 min twice daily
Stimulation site	Left cymba conchae	Left cymba conchae

The migraine literature shows a striking contrast with the epilepsy literature:

In epilepsy: 25 Hz outperforms 1 Hz
In migraine: 1 Hz appears to outperform 25 Hz

This frequency-dependent difference may reflect distinct pathophysiological targets. Epilepsy requires modulation of cortical excitability (favoured by higher-frequency stimulation of locus coeruleus norepinephrine pathways), while migraine may benefit more from modulation of descending serotonergic inhibition and trigeminovascular processing (potentially favoured by lower frequencies). This is an important observation for clinical practice, though it is based on a single trial and further dose-response studies are needed.

The Clinical Evidence: What Do the Trials Show?

This is the section that matters most for clinicians making decisions. The evidence comes from two distinct approaches: auricular tVNS (targeting the ear) and cervical tVNS (targeting the neck). Both are relevant because they establish that vagal neuromodulation has genuine effects on migraine.

Auricular tVNS Evidence

Straube et al. (2015): The Key Auricular Trial

This randomised, double-blind trial is the most directly relevant study for auricular tVNS in chronic migraine. After a 1-month baseline, chronic migraine patients were randomised to 25 Hz or 1 Hz stimulation at the left cymba conchae using the NEMOS/tVNS device, 4 hours daily for 3 months.

Results (per protocol, n=40):

1 Hz group: reduction of 7.0 ± 4.6 headache days per 28 days
25 Hz group: smaller reduction (1 Hz significantly larger, p < 0.05)
Both groups showed significant improvements in HIT-6 and MIDAS disability scores
Both groups reduced acute medication intake

The mean reduction of 7 headache days per 28 days in the 1 Hz group exceeds what has been reported for other nerve stimulation procedures in chronic migraine. However, this trial compared two active frequencies rather than active versus sham, so the absolute treatment effect size cannot be determined. It is an important limitation, and one that should be stated clearly.

Migraine-Specific fMRI Studies

Zhang et al. (2019) and Chen et al. (2023) provided mechanistic validation for the auricular approach in migraine, demonstrating brainstem pathway engagement and functional connectivity changes that correlated with clinical improvement.

Cervical tVNS (gammaCore) Evidence

The cervical approach has a larger clinical trial programme for migraine, and this evidence strengthens the overall case for vagal neuromodulation.

PRESTO Trial (Tassorelli et al., 2018): Acute Treatment

The most rigorous RCT for acute migraine treatment with nVNS. 248 patients with episodic migraine across 10 Italian centres.

Primary endpoint (2-hour pain freedom): nVNS 30.4% vs sham 19.7% (p=0.067, not significant)
30-minute pain freedom: 12.7% vs 4.2% (p=0.012, significant)
60-minute pain freedom: 21.0% vs 10.0% (p=0.023, significant)
No serious adverse events

PREMIUM Trial (Diener et al., 2019): Episodic Prevention

Multicentre, double-blind, sham-controlled trial. 332 patients with episodic migraine in the ITT analysis.

Primary endpoint (migraine day reduction): nVNS -2.26 vs sham -1.80 (p=0.15, not significant)
Modified ITT (≥67% adherence, n=278): migraine days nVNS -2.27 vs sham -1.53 (p=0.043, significant); acute medication days nVNS -1.94 vs sham -1.14 (p=0.039, significant)

The adherence-dependent result is important: patients who used the device consistently showed significantly better outcomes.

PREMIUM II Trial (Najib et al., 2022): Episodic Prevention

Follow-up sham-controlled trial. Closed early (231 of 400 planned) due to COVID-19.

Monthly headache days: nVNS -4.6 vs sham -3.0 (p=0.05, significant)
50% responder rate: nVNS 44.87% vs sham 26.81% (p=0.05, significant)
Migraine with aura subgroup: nVNS -5.5 vs sham -2.7 headache days (p < 0.05)

Despite early closure, PREMIUM II demonstrated significant superiority for nVNS over sham, with a particularly strong effect in migraine with aura.

What the Meta-Analyses Tell Us

The Zhuo et al. (2023) meta-analysis of 6 RCTs (845 patients) is particularly important because it analysed auricular and cervical approaches separately:

Low-frequency auricular nVNS: significant reduction in monthly headache days (MD -1.8, p=0.02) and headache intensity (SMD -0.7, p=0.009)
Cervical nVNS: not significant for headache day reduction (MD -0.46, p=0.23)
Overall 50% responder rate: OR 1.69 (p=0.009, significant)

This meta-analytic finding that low-frequency auricular nVNS significantly reduces headache days and intensity while cervical nVNS does not reach significance for headache day reduction is noteworthy. It suggests that the auricular approach may have distinct advantages for migraine prevention.

The International Headache Society 2025 evidence-based guidelines gave gammaCore a weak recommendation for preventive migraine treatment. No formal recommendation was issued for auricular tVNS devices due to insufficient qualifying RCTs, though the guidelines described non-invasive neuromodulation devices as "promising alternatives to drug treatment" that are "safe and generally well tolerated and devoid of drug interactions."

KEY POINT: The clinical evidence for tVNS in migraine includes one auricular RCT showing a 7-day reduction in headache days at 1 Hz in chronic migraine, multiple cervical nVNS trials demonstrating significant acute and preventive effects, and a meta-analysis confirming that low-frequency auricular stimulation significantly reduces headache days and intensity. The evidence is at an earlier stage than for epilepsy or depression, but the mechanistic rationale is strong, the cervical nVNS data is substantial, and the meta-analytic signal for auricular tVNS is clear.

How Does tVNS Compare with Other Preventive Treatments?

No head-to-head trials exist, so the following comparison uses cross-study data and must be interpreted with caution.

Treatment	50% Responder Rate	Mean Day Reduction	Route	Setting
OnabotulinumtoxinA (PREEMPT)	~45% at 24 weeks	~8 days at 56 weeks	Injection	Clinic
Erenumab 140mg	~40 to 50% at 12 weeks	~6 days	SC injection	Home/clinic
Fremanezumab 225mg	~38 to 41% at 12 weeks	~5 days	SC injection	Home/clinic
Topiramate 100mg	~35 to 45%	~2 to 3 days	Oral daily	Home
Cervical nVNS (PREMIUM II)	44.87%	~4.6 days (episodic)	Neck device	Home
Auricular tVNS 1 Hz (Straube)	Not reported vs sham	~7 days (no sham arm)	Ear electrode	Home

Important caveat: The Straube auricular tVNS data lacks a true sham arm, so the 7-day reduction includes placebo effect. The PREMIUM trials studied episodic (not chronic) migraine. Cross-study comparisons are inherently limited.

tVNS offers distinctive advantages: it is non-invasive, home-based, self-administered, has no drug interactions, no systemic side effects, no medication overuse risk, and substantially lower cost than CGRP monoclonal antibodies or onabotulinumtoxinA. It can be used alongside any pharmacological treatment.

KEY POINT: tVNS is not a replacement for established treatments. It is an additional option, particularly suited to patients who have not responded adequately to preventive medication, who cannot tolerate pharmacological side effects, or who want to reduce their reliance on acute medication. Its safety profile is arguably the best of any migraine preventive approach.

Safety Profile

One of the most compelling aspects of tVNS is its safety record. Across all published migraine trials for both auricular and cervical approaches, no serious device-related adverse events have been reported.

Common, mild and transient:

Local skin effects: tingling, itching, erythema at electrode site
Headache
Ear discomfort

Uncommon:

Tinnitus (resolves on cessation)
Dizziness, facial muscle twitching (cervical approach)

A systematic review and meta-analysis of 177 studies involving 6,322 subjects found no significant difference in the risk of adverse events between taVNS and control groups (Redgrave et al., 2018). In the PREMIUM trial, dropout due to adverse events was actually lower in the active nVNS group (1.2%) than the sham group (5.2%).

By comparison, topiramate causes cognitive dysfunction, paraesthesia, and weight loss in a significant proportion of patients. CGRP monoclonal antibodies cause constipation (erenumab, up to 17.9%) and injection site reactions. OnabotulinumtoxinA causes injection site pain and muscle weakness. Beta-blockers cause fatigue, cold extremities, and are contraindicated in asthma.

The safety advantage of tVNS over all pharmacological preventive options is substantial and consistent.

Regulatory and Access Context

The tVNS® E device (tVNS Technologies GmbH, Germany) received CE marking in 2010 and now holds Class IIa certification under EU-MDR 2017/745, verified by TÜV SÜD. The EU-MDR approval covers migraine as a specific, approved indication.

The gammaCore® (electroCore) holds FDA clearance for both acute and preventive treatment of migraine in adults, as well as acute and preventive treatment of cluster headache. It is also CE-marked for primary headaches including migraine, cluster headache, and medication overuse headache.

For UK practice, NICE IPG652 (2019) covers transcutaneous stimulation of the cervical branch of the vagus nerve for cluster headache, but there is no specific NICE guidance for tVNS (auricular or cervical) for migraine. NICE CG150 (Headaches in over 12s) does not currently include tVNS in its migraine prevention recommendations. Given the CE marking under EU-MDR 2017/745, tVNS can be used in UK clinical practice for migraine, though formal NICE guidance specific to tVNS for migraine is currently lacking.

The IHS 2025 evidence-based guidelines gave gammaCore a weak recommendation for preventive migraine treatment. No formal recommendation was issued for auricular tVNS devices.

Predicting Response: Who Benefits Most?

Migraine with Aura

The most consistently identified predictive factor. PREMIUM II showed that migraine with aura patients achieved a 5.5-day reduction in headache days vs 2.7 for sham (p < 0.05), representing more than 100% therapeutic gain. This is mechanistically consistent with the CSD-inhibiting properties of VNS.

Adherence

The PREMIUM trial demonstrated that adherent patients (≥67% usage) show significantly better outcomes than the general ITT population. Consistent daily use is a key determinant of treatment success.

fMRI-Based Prediction

Early fractional amplitude of low-frequency fluctuation (fALFF) patterns can predict taVNS treatment efficacy in migraine without aura (published 2022). Machine learning approaches using resting-state fMRI have demonstrated feasibility of neuroimaging-guided patient selection, though these are not yet clinically practical.

Beyond Headache Days: Comorbidity Benefits

Migraine rarely exists in isolation, and tVNS has shown benefits across several common comorbidities:

Medication overuse: tVNS provides pain management without contributing to MOH and may facilitate acute medication reduction. The PREMIUM mITT analysis showed significant reduction in acute medication days. gammaCore holds CE marking for medication overuse headache.
Mood: Depression and anxiety are 2 to 5 times more prevalent in chronic migraine. The tVNS system holds EU-MDR approval for both depression and anxiety. The monoaminergic mechanisms engaged by tVNS are directly relevant to both migraine and mood disorders.
Sleep: Migraine and sleep disturbance have a bidirectional relationship. Kinfe et al. (2015) specifically documented improvements in migraine-associated sleep disturbance with nVNS.
Autonomic symptoms: Vagal modulation of autonomic regulation may directly address nausea, rhinorrhoea, and lacrimation associated with migraine attacks.

What We Don't Yet Know

Here are the key unanswered questions:

No large sham-controlled RCT for auricular tVNS in chronic migraine. The Straube 2015 trial compared two active frequencies rather than active versus sham. This is the single most important evidence gap for the auricular approach.

Optimal auricular parameters for migraine are not established by dose-response studies. The finding that 1 Hz outperforms 25 Hz (opposite to epilepsy) needs replication.

Long-term outcomes: No controlled data beyond 3 months for auricular tVNS in migraine. The EVENT open-label extension suggests sustained benefit at 8 months but is uncontrolled.

Head-to-head comparisons: No trials comparing tVNS with CGRP monoclonal antibodies, onabotulinumtoxinA, or rTMS for migraine.

Auricular vs cervical comparison: No head-to-head trial comparing the two tVNS approaches.

Chronic migraine specifically: Most cervical nVNS trials enrolled episodic migraine patients. The chronic migraine evidence base is more limited.

Paediatric migraine: A protocol for a randomised trial of taVNS for primary headache in children and adolescents was published in BMJ Open (2025), but results are pending.

Practical Guidance for Clinicians

For UK clinicians considering taVNS in migraine management, the following practical points are relevant.

Candidate Selection

Adults with chronic migraine (≥15 headache days/month) who have not responded adequately to at least one preventive medication
Patients with episodic migraine seeking non-pharmacological prevention, particularly those with migraine with aura
Patients at risk of or already experiencing medication overuse headache
Patients unable to access or tolerate CGRP-targeted therapies or onabotulinumtoxinA
Absence of cardiac pacemakers or implanted metallic devices near the ear
Exclusion of severe cardiac arrhythmia

Treatment Initiation

Establish a baseline headache diary (minimum 4 weeks recommended)
Based on the Straube protocol: 1 Hz, 250 µs pulse width, maximum tolerated intensity, 4 hours daily at the left cymba conchae
Alternative shorter protocol: 30 minutes twice daily at similar parameters
Assess response at 4, 8, and 12 weeks using headache diary (migraine days, headache days, acute medication days)
Allow at least 12 weeks before judging response

What to Tell Your Patients

Based on available evidence, low-frequency auricular tVNS can significantly reduce headache days and headache intensity. The strongest evidence comes from a chronic migraine trial showing an average reduction of 7 headache days per month.
The benefit builds over time. Allow at least 8 to 12 weeks of consistent use before judging response.
If you experience migraine with aura, you may be particularly likely to respond.
Mild local side effects (tingling at the electrode site) are expected and well tolerated.
The device does not contribute to medication overuse and can be used alongside any existing treatment.
Building sessions into a daily routine (while reading, watching television, or resting) helps with adherence, and adherence is strongly associated with better outcomes.

Comorbidity Considerations

Depression and anxiety are extremely common in chronic migraine. The dual benefit of tVNS for headache and mood is clinically attractive. Medication overuse headache may also improve as patients reduce acute medication reliance.

Conclusion

The most honest summary is this: transcutaneous vagus nerve stimulation is a mechanistically well-grounded, safe, and clinically encouraging approach to migraine management. The neurobiological rationale is strong and converging, with multiple animal and human studies demonstrating inhibition of cortical spreading depression, suppression of trigeminocervical nociception, reduction of CGRP expression, and modulation of descending pain inhibitory pathways.

The clinical evidence comes from two complementary approaches. Cervical nVNS (gammaCore) has the larger trial programme, with significant results for acute treatment (PRESTO) and episodic migraine prevention (PREMIUM II), and FDA clearance for both indications. Auricular tVNS at 1 Hz has shown a 7-day reduction in headache days in chronic migraine (Straube 2015), and meta-analytic evidence confirms that low-frequency auricular stimulation significantly reduces headache days and intensity.

The auricular tVNS evidence base for migraine is at an earlier stage than for epilepsy or depression. The critical gap is the absence of a large, sham-controlled RCT for auricular tVNS in chronic migraine. This should be stated clearly.

What the evidence does support is that tVNS is safe, well-tolerated, biologically rational, and has a credible body of clinical and mechanistic data. As a CE-marked Class IIa medical device with regulatory approval for migraine, it represents a legitimate clinical option. Its safety profile is arguably the best of any migraine preventive approach. Its accessibility (home-based, self-administered), absence of drug interactions, inability to cause medication overuse, and low cost make it especially appealing for patients who have not responded to or cannot tolerate pharmacological options.

Related Literature

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Oshinsky ML, Murphy AL, Hekierski H, Cooper M, Simon BJ. Noninvasive vagus nerve stimulation as treatment for trigeminal allodynia. Pain. 2014;155(5):1037-1042.
Frangos E, Ellrich J, Komisaruk BR. Non-invasive access to the vagus nerve central projections via electrical stimulation of the external ear: fMRI evidence in humans. Brain Stimul. 2015;8(3):624-636.
Kinfe TM, Pintea B, Muhammad S, et al. Cervical non-invasive vagus nerve stimulation (nVNS) for preventive and acute treatment of episodic and chronic migraine and migraine-associated sleep disturbance. J Headache Pain. 2015;16:101.
Straube A, Ellrich J, Eren O, Blum B, Ruscheweyh R. Treatment of chronic migraine with transcutaneous stimulation of the auricular branch of the vagal nerve (auricular t-VNS): a randomized, monocentric clinical trial. J Headache Pain. 2015;16:543.
Chen SP, Ay I, de Morais AL, et al. Vagus nerve stimulation inhibits cortical spreading depression. Pain. 2016;157(4):797-805.
Silberstein SD, Calhoun AH, Lipton RB, et al. Chronic migraine headache prevention with noninvasive vagus nerve stimulation: The EVENT study. Neurology. 2016;87(5):529-538.
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Review current as of April 2026. Based on evidence available up to and including early 2026.