Acute Brain InjuryNCT07384845
The Role of Transcutaneous Vagus Nerve Stimulation in Treatment of Acute Brain Injury
A study testing transcutaneous vagus nerve stimulation (tVNS) in people with Acute Brain Injury and Transcutaneous Vagus Nerve Stimulation, run by Clinical Hospital Centre Zagreb at 1 site in Croatia.
Trial summary
Acute brain injury is a major global health problem associated with high mortality and morbidity, limited therapeutic options, prolonged hospital stays, and long-term disability that significantly impairs quality of life and increases healthcare costs. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Acute Brain Injury, Transcutaneous Vagus Nerve Stimulation, Neuromodulation
- What is being tested?
- transcutaneous vagus nerve stimulation (tVNS)
- Type of treatment
- Medical device
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 60 participants
- Where
- 1 siteCroatia
- Study dates
- Feb 2026to Feb 2028
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
None listed.
Who cannot join
- Patients under 18 years of age; patients with autoimmune diseases or malignant diseases; pregnant women; and patients for whom informed consent to participate in the study is not obtained.
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
About this study
Official title: The Role of Transcutaneous Vagus Nerve Stimulation in Neuroprotection and the Reduction of the Systemic Inflammatory Response in Acute Brain Injury
Acute brain injury is a major global health problem associated with high mortality and morbidity, limited therapeutic options, prolonged hospital stays, and long-term disability that significantly impairs quality of life and increases healthcare costs. Noninvasive transcutaneous VNS developed as a safer approach for treating cerebral edema, epileptic seizures, and blood-brain barrier disruption, for facilitating the recovery of motoric and cognitive functions, and for immunomodulation.
Transcutaneous VNS improves cerebral perfusion pressure and tissue oxygenation, supports reperfusion of the penumbral zone, and reduces neuronal hyperexcitability, thereby suppressing seizures.It may exert anti-inflammatory effects by reducing microglial cytokine and chemokine production. Additionally, vagal stimulation promotes acetylcholine-mediated suppression of pro-inflammatory cytokines, including TNF, IL-1β, IL-6, and IL-18.
Read more
Another anti-inflammatory mechanism involves ghrelin, a peptide hormone whose serum levels increase under vagal stimulation. Elevated ghrelin reduces TNF-α and other pro-inflammatory cytokines and may limit intracerebral hemorrhage by inhibiting the NLRP3 inflammasome and activating the Nrf2/ARE signaling pathway. Biomarkers such as S100 protein and neuron-specific enolase (NSE) are valuable indicators of brain tissue damage and clinical outcomes; tVNS may reduce their levels and support non-invasive monitoring of disease progression.
The technique is considered safe in patients .
To date, tVNS has not been evaluated in clinical trials in Croatia, nor reported in case studies or cohort analyses. Study outcomes will be correlated with patients' clinical status, duration and course of hospitalization, complication rates, and overall treatment outcomes.
Read the detailed description
Acute brain injury is one of the leading health problems of today. It presents with high mortality and morbidity, limited therapeutic options, and prolonged hospital stays, leaving patients with disabilities that impair quality of life and increase healthcare costs. The etiology of brain injury may be traumatic or non-traumatic. The global incidence of traumatic brain injury (TBI) is estimated at 27 to 69 million cases per year, mainly due to falls and traffic accidents. Among the most challenging non-traumatic brain injuries is aneurysmal subarachnoid hemorrhage (aSAH), with an incidence of 10-15 patients per 100,000 per year. In the treatment of primary and secondary brain injury, both surgical and non-surgical procedures are important. Limited therapeutic options in the treatment of brain injury have opened the door to consideration of new non-invasive methods. Recent studies show that neuromodulation induced by vagus nerve stimulation (VNS) may contribute to better outcomes in patients with brain injury.
The first application of VNS in a clinical setting was an invasive procedure used in the treatment of pharmacoresistant epilepsy. Subsequently, a non-invasive method of transcutaneous VNS (tVNS) was developed, which may have neuroprotective and immunoprotective effects. According to existing research, tVNS provides a safer approach in the treatment of cerebral edema, epileptic seizures, disorders of the cerebral blood-brain barrier, recovery of motor and cognitive functions, and immunomodulation. Transcutaneous VNS induces enhanced regulation of endogenous noradrenergic activity through activation of the locus coeruleus and the release of noradrenaline in the amygdala, as well as higher overall concentrations of noradrenaline in the brain. Accordingly, an increase in cerebral perfusion pressure (CPP) enables better oxygenation of brain tissue and reperfusion of the penumbral zone. Noradrenaline suppresses seizures by protecting GABAergic neurons and reducing neuronal hyperexcitability. In addition, it exerts anti-inflammatory effects on microglial cells, reducing the production of cytokines and chemokines. Acetylcholine (ACh), under vagal stimulation, also reduces pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukins IL-1β, IL-6, and IL-18. At the same time, it influences the microglial phenotype, reducing the pro-inflammatory M1 microglial phenotype, which promotes oxidative stress and mitochondrial damage, in favor of the neuroprotective M2 phenotype. Recent studies show that tVNS also significantly modulates serum inflammatory cytokines in patients with sepsis. Another anti-inflammatory mechanism is the interaction of VNS with the peptide hormone ghrelin. Serum ghrelin concentrations increase under vagal stimulation, leading to a subsequent reduction in TNF-α levels and other pro-inflammatory cytokines after brain injury. Ghrelin also plays an important role in reducing intracerebral hemorrhage by inhibiting NLRP3 and stimulating the Nrf2/ARE signaling pathway. Analysis of biomarkers of brain tissue damage, such as S100 protein and neuron-specific enolase (NSE), can be used to assess mortality and morbidity, as well as outcomes of neurointensive care, and non-invasive tVNS stimulation could result in a reduction of their values and serve in monitoring the clinical condition of patients with brain injury.
Motor recovery depends on brain neuroplasticity, and the results of previous studies indicate significantly better functional motor recovery when rehabilitation therapy is combined with tVNS. Non-invasive tVNS can also alleviate cognitive dysfunction, as it reduces neuroinflammation and improves memory function through stimulation of peripheral and central cholecystokinin (CCK) receptors.
The use of tVNS is safe in patients with aSAH and stroke, and it significantly improves functional recovery in patients in a minimally conscious state after transauricular tVNS administered for a duration of four weeks.
To the best of our knowledge, tVNS has not yet been used in clinical trials in Croatia, nor has it been described in case reports or small cohort studies. The obtained results will be correlated with collected data on patients' clinical status, the course and duration of hospital treatment, the occurrence of complications, and treatment outcomes.
- Conditions
- Acute Brain Injury, Transcutaneous Vagus Nerve Stimulation, Neuromodulation, Immunomodulation
- Being tested
- transcutaneous vagus nerve stimulation (tVNS), Sham (No Treatment)
- Medical subject headings
- Brain Injuries
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
transcutaneous vagus nerve stimulation (tVNS)Device
application of tVNS in patients with acute brain injury
Sham (No Treatment)Device
TVNS will be placed in the same manner as in the first group, but without vagal stimulation
| Study group | Role | What they receive |
|---|---|---|
| Acute brain injury patients with tVNS stimulation | Active comparator | tVNS will be applied on left tragus, followed by stimulation with 20 Hz twice daily.
Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP), ghrelin and cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) will be measured on two occasions. CT angiography on the first and seventh day for patients with SAH. Receives: Device: transcutaneous vagus nerve stimulation (tVNS) |
| Acute brain injury patients with sham | Sham comparator | tVNS VNS will be applied on left tragus, but without stimulation in the same time frame as in the first group. Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP), ghrelin and cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) will be measured on two occasions. CT angiography on the first and seventh day for patients with SAH. Receives: Device: Sham (No Treatment) |
What is being measured
The primary outcome is the main question the study is designed to answer.
Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP) and ghrelin
To measure and analyze the concentrations of biomarkers of traumatic brain injury (S100B, neuron-specific enolase [NSE], GFAP) as well as the peptide hormone ghrelin, in serum and cerebrospinal fluid within 24 hours of admission to the intensive care unit (ICU), and again after 7 days.
Measured: 7 days
Cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10)
To measure and analyze concentration of cytokines in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) within 24 hours of admission to the intensive care unit (ICU), and again after 7 days
Measured: 7 days
CT angiography in patients with aneurysmatic SAH
Radiologically monitor the presence, development, and severity of vasospasm in patients with aSAH using CT angiography on two occasions: within 24 hours of the ruptured aneurysm closure, and on the 7th day after aneurysm closure
Measured: 7 days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Feb 2026
- Study startFeb 2026 (estimated)
- Primary completionFeb 2028 (estimated)
- Study completionFeb 2028 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Acute Brain InjuryStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Other
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Care provider
- Enrolment
- 60 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Clinical Hospital Centre Zagreb
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Dinko Tonković, Clinical Hospital Centre Zagreb
- Investigators
- Dinko Tonković, Prof, MD PhD, Principal investigator, Clinical Hospital Centre ZagrebMartina Miklić Bublić, MD PhD, Principal investigator, Clinical Hospital Centre ZagrebDunja Rogić, Prof, MD PhD, Principal investigator, Clinical Hospital Centre Zagreb
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07384845
- Sponsor's protocol ID
- 02/013AG
- Status last verified
- Jan 2026
- First submitted
- 26 Jan 2026
- Last updated
- 3 Feb 2026
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 3 Feb 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Role of Transcutaneous Vagus Nerve Stimulation in Neuroprotection and the Reduction of the Systemic Inflammatory Response in Acute Brain Injury
- ClinicalTrials.gov ID
- NCT07384845
- Acronym / sponsor ID
- 02/013AG
- Conditions
- Acute Brain Injury, Transcutaneous Vagus Nerve Stimulation, Neuromodulation, Immunomodulation
- Study type
- Interventional
- Recruitment status
- Not yet recruiting
- Enrolment
- 60 participants (estimated)
- Lead sponsor
- Clinical Hospital Centre ZagrebUniversity, hospital or other
- Study start
- Feb 2026 (estimated)
- Primary completion
- Feb 2028 (estimated)
- Study completion
- Feb 2028 (estimated)
- First posted
- 3 Feb 2026 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Acute brain injury is a major global health problem associated with high mortality and morbidity, limited therapeutic options, prolonged hospital stays, and long-term disability that significantly impairs quality of life and increases healthcare costs. Noninvasive transcutaneous VNS developed as a safer approach for treating cerebral edema, epileptic seizures, and blood-brain barrier disruption, for facilitating the recovery of motoric and cognitive functions, and for immunomodulation.
Transcutaneous VNS improves cerebral perfusion pressure and tissue oxygenation, supports reperfusion of the penumbral zone, and reduces neuronal hyperexcitability, thereby suppressing seizures.It may exert anti-inflammatory effects by reducing microglial cytokine and chemokine production. Additionally, vagal stimulation promotes acetylcholine-mediated suppression of pro-inflammatory cytokines, including TNF, IL-1β, IL-6, and IL-18.
Another anti-inflammatory mechanism involves ghrelin, a peptide hormone whose serum levels increase under vagal stimulation. Elevated ghrelin reduces TNF-α and other pro-inflammatory cytokines and may limit intracerebral hemorrhage by inhibiting the NLRP3 inflammasome and activating the Nrf2/ARE signaling pathway. Biomarkers such as S100 protein and neuron-specific enolase (NSE) are valuable indicators of brain tissue damage and clinical outcomes; tVNS may reduce their levels and support non-invasive monitoring of disease progression.
The technique is considered safe in patients .
To date, tVNS has not been evaluated in clinical trials in Croatia, nor reported in case studies or cohort analyses. Study outcomes will be correlated with patients' clinical status, duration and course of hospitalization, complication rates, and overall treatment outcomes.
Detailed description
Acute brain injury is one of the leading health problems of today. It presents with high mortality and morbidity, limited therapeutic options, and prolonged hospital stays, leaving patients with disabilities that impair quality of life and increase healthcare costs. The etiology of brain injury may be traumatic or non-traumatic. The global incidence of traumatic brain injury (TBI) is estimated at 27 to 69 million cases per year, mainly due to falls and traffic accidents. Among the most challenging non-traumatic brain injuries is aneurysmal subarachnoid hemorrhage (aSAH), with an incidence of 10-15 patients per 100,000 per year. In the treatment of primary and secondary brain injury, both surgical and non-surgical procedures are important. Limited therapeutic options in the treatment of brain injury have opened the door to consideration of new non-invasive methods. Recent studies show that neuromodulation induced by vagus nerve stimulation (VNS) may contribute to better outcomes in patients with brain injury.
The first application of VNS in a clinical setting was an invasive procedure used in the treatment of pharmacoresistant epilepsy. Subsequently, a non-invasive method of transcutaneous VNS (tVNS) was developed, which may have neuroprotective and immunoprotective effects. According to existing research, tVNS provides a safer approach in the treatment of cerebral edema, epileptic seizures, disorders of the cerebral blood-brain barrier, recovery of motor and cognitive functions, and immunomodulation. Transcutaneous VNS induces enhanced regulation of endogenous noradrenergic activity through activation of the locus coeruleus and the release of noradrenaline in the amygdala, as well as higher overall concentrations of noradrenaline in the brain. Accordingly, an increase in cerebral perfusion pressure (CPP) enables better oxygenation of brain tissue and reperfusion of the penumbral zone. Noradrenaline suppresses seizures by protecting GABAergic neurons and reducing neuronal hyperexcitability. In addition, it exerts anti-inflammatory effects on microglial cells, reducing the production of cytokines and chemokines. Acetylcholine (ACh), under vagal stimulation, also reduces pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukins IL-1β, IL-6, and IL-18. At the same time, it influences the microglial phenotype, reducing the pro-inflammatory M1 microglial phenotype, which promotes oxidative stress and mitochondrial damage, in favor of the neuroprotective M2 phenotype. Recent studies show that tVNS also significantly modulates serum inflammatory cytokines in patients with sepsis. Another anti-inflammatory mechanism is the interaction of VNS with the peptide hormone ghrelin. Serum ghrelin concentrations increase under vagal stimulation, leading to a subsequent reduction in TNF-α levels and other pro-inflammatory cytokines after brain injury. Ghrelin also plays an important role in reducing intracerebral hemorrhage by inhibiting NLRP3 and stimulating the Nrf2/ARE signaling pathway. Analysis of biomarkers of brain tissue damage, such as S100 protein and neuron-specific enolase (NSE), can be used to assess mortality and morbidity, as well as outcomes of neurointensive care, and non-invasive tVNS stimulation could result in a reduction of their values and serve in monitoring the clinical condition of patients with brain injury.
Motor recovery depends on brain neuroplasticity, and the results of previous studies indicate significantly better functional motor recovery when rehabilitation therapy is combined with tVNS. Non-invasive tVNS can also alleviate cognitive dysfunction, as it reduces neuroinflammation and improves memory function through stimulation of peripheral and central cholecystokinin (CCK) receptors.
The use of tVNS is safe in patients with aSAH and stroke, and it significantly improves functional recovery in patients in a minimally conscious state after transauricular tVNS administered for a duration of four weeks.
To the best of our knowledge, tVNS has not yet been used in clinical trials in Croatia, nor has it been described in case reports or small cohort studies. The obtained results will be correlated with collected data on patients' clinical status, the course and duration of hospital treatment, the occurrence of complications, and treatment outcomes.
Study design
- Primary purpose
- Other
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, care provider)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Acute brain injury patients with tVNS stimulation | Active comparator | Device: transcutaneous vagus nerve stimulation (tVNS)tVNS will be applied on left tragus, followed by stimulation with 20 Hz twice daily. Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP), ghrelin and cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) will be measured on two occasions. CT angiography on the first and seventh day for patients with SAH. |
| Acute brain injury patients with sham | Sham comparator | Device: Sham (No Treatment)tVNS VNS will be applied on left tragus, but without stimulation in the same time frame as in the first group. Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP), ghrelin and cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) will be measured on two occasions. CT angiography on the first and seventh day for patients with SAH. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (0 listed)
Key exclusion criteria (1 listed)
- Patients under 18 years of age; patients with autoimmune diseases or malignant diseases; pregnant women; and patients for whom informed consent to participate in the study is not obtained.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| transcutaneous vagus nerve stimulation (tVNS)application of tVNS in patients with acute brain injury | Device | Acute brain injury patients with tVNS stimulation |
| Sham (No Treatment)TVNS will be placed in the same manner as in the first group, but without vagal stimulation | Device | Acute brain injury patients with sham |
Primary outcome
Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP) and ghrelin
Time frame: 7 days
To measure and analyze the concentrations of biomarkers of traumatic brain injury (S100B, neuron-specific enolase [NSE], GFAP) as well as the peptide hormone ghrelin, in serum and cerebrospinal fluid within 24 hours of admission to the intensive care unit (ICU), and again after 7 days.
Cytokine concentrations in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10)
Time frame: 7 days
To measure and analyze concentration of cytokines in serum and cerebrospinal fluid (IL-1β, IL-6, TNF-α, IL-10) within 24 hours of admission to the intensive care unit (ICU), and again after 7 days
CT angiography in patients with aneurysmatic SAH
Time frame: 7 days
Radiologically monitor the presence, development, and severity of vasospasm in patients with aSAH using CT angiography on two occasions: within 24 hours of the ruptured aneurysm closure, and on the 7th day after aneurysm closure
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Feb 2026.
- Individual participant dataSharing planned: No
Related trials for Acute Brain Injury
RecruitingObservational study
Sleep to Predict Recovery In Unconscious Patients With Acute Brain Injury
Traumatic Brain Injury (TBI) Patients, Intracerebral Hemorrhage (ICH)
Recruiting
The Coma Family Program (COMA-F): A Resilience Program for Caregivers of Patients With Severe Acute Brain Injury
Caregiver Distress, Emotional Distress
Recruiting
Rapid Local Ischemic Postconditioning on Stroke After Thrombectomy
Acute Ischemic Stroke
Enrolling by invitation
Fareon Open Label Device Clinical Trial
Cognitive Dysfunction, Acquired Brain Injury
Not yet recruiting
Supplementary Neuromuscular Rehabilitation During Acute Concussion Recovery
Concussion (Diagnosis), Gait Abnormality
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Dinko Tonković, Prof, MD PhD principal investigator
Clinical Hospital Centre Zagreb
Martina Miklić Bublić, MD PhD principal investigator
Clinical Hospital Centre Zagreb
Dunja Rogić, Prof, MD PhD principal investigator
Clinical Hospital Centre Zagreb
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing transcutaneous vagus nerve stimulation (tVNS) in people with Acute Brain Injury and Transcutaneous Vagus Nerve Stimulation, run by Clinical Hospital Centre Zagreb at 1 site in Croatia.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 0 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 3 Feb 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Croatia. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Biomarkers of traumatic brain injury (S100B, neuron-specific enolase, GFAP) and ghrelin (time frame: 7 days). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 Feb 2026.