Subarachnoid Hemorrhage
Conditions
Keywords
Vagal nerve stimulation
Brief summary
This study will evaluate whether non-invasive auricular vagal nerve stimulation lowers inflammatory markers, and improves outcomes following spontaneous subarachnoid hemorrhage.
Detailed description
Vagal nerve stimulation (VNS) has been studied in several inflammatory conditions, and has been implemented in animal models of subarachnoid hemorrhage (SAH) with promising results. The purpose of the proposed study is to determine how applying auricular VNS in patients presenting with spontaneous SAH impacts their expression of inflammatory markers in their blood and cerebrospinal fluid (CSF), and how it impacts their clinical course and outcomes. This study will involve randomizing patients to stimulation with VNS, or sham stimulation. Blood and CSF will be collected on admission, and serially throughout the patient's admission. Clinical events tracked during the hospital stay include development of cerebral vasospasm, need for CSF diversion via a shunt, stress-induced cardiomyopathy, and development of stroke or global cerebral ischemia. Outcomes following admission will include functional scores at discharge, and at follow-up visits for up to 2 years after discharge.
Interventions
Transcutaneous auricular vagal nerve stimulation
Transcutaneous auricular vagal nerve ear clip applied without current
Sponsors
Anna Huguenard
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
TRIPLE (Subject, Caregiver, Outcomes Assessor)
Masking description
All participants will be fitted with an auricular stimulator, but blinded to whether they are receiving stimulation or not. Outcome scores will be assessed and recorded by clinicians blinded to treatment arm.
Intervention model description
Participants are assigned to either stimulation or sham stimulation arms
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Spontaneous subarachnoid hemorrhage
Exclusion criteria
* Trauma-induced subarachnoid hemorrhage * Ongoing chemotherapy * Taking immunosuppressive medications for other medical illnesses * Presence of a pacemaker * Prolonged bradycardia at time of admission
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Inflammatory markers in the serum on admission | On hospital day 1 | TNF alpha from blood draw |
| Change in inflammatory markers in the serum | Through hospital admission, average of 4 weeks | TNF alpha from blood draws |
| Inflammatory markers in the CSF on admission | On hospital day 1 | TNF alpha from cerebrospinal fluid |
| Change in inflammatory markers in the CSF | Through hospital admission, average of 4 weeks | TNF alpha from cerebrospinal fluid |
| Cerebral vasospasm | Through hospital admission, average of 4 weeks | Presence of moderate/severe radiographic vasospasm |
| Hydrocephalus | Through hospital admission, average of 4 weeks | Need for permanent CSF diversion via a ventricular shunt |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Change in inflammatory markers in the CSF | Through hospital admission, average of 4 weeks | IL-12, GM-CSF, IFN gamma, IL-1b, IL-10, IL-13, IL-17A, IL-2, IL-4, IL-5, IL-6, IL-8, from cerebrospinal fluid |
| Clinical outcome | 2 years | Modified Rankin Scale for Neurological Disability (minimum score 0, maximum score 6, better outcomes have lower scores) |
| Cerebral vasospasm | Through hospital admission, average of 4 weeks | Additional features of vasospasm: 1) Number of vascular studies obtained, 2) Need for blood pressure augmentation or hypervolemia, 3) Need for intraarterial or intrathecal vasodilator, 4) Need for angioplasty |
| Cerebral ischemia | Through hospital admission, average of 4 weeks | Presence of cerebral ischemia based on the following criteria: Radiographic evidence of a new infarct or stroke |
| Hydrocephalus | Through hospital admission, average of 4 weeks | Duration of temporary CSF diversion via an external ventricular drain |
| Inflammatory markers in the serum on admission | On hospital day 1 | IL-12, GM-CSF, IFN gamma, IL-1b, IL-10, IL-13, IL-17A, IL-2, IL-4, IL-5, IL-6, IL-8from blood draws |
| Change in inflammatory markers in the serum | Through hospital admission, average of 4 weeks | IL-12, GM-CSF, IFN gamma, IL-1b, IL-10, IL-13, IL-17A, IL-2, IL-4, IL-5, IL-6, IL-8 from blood draws |
| Inflammatory markers in the CSF on admission | On hospital day 1 | IL-12, GM-CSF, IFN gamma, IL-1b, IL-10, IL-13, IL-17A, IL-2, IL-4, IL-5, IL-6, IL-8, from cerebrospinal fluid |
| Stressed-induced cardiomyopathy | Through hospital admission, average of 4 weeks | Presence of stressed-induced cardiomyopathy based on any of the following criteria: 1) New troponin elevation, 2) New EKG changes (specifically ST segment elevation, ST segment depression, left bundle branch block, prolonged QT interval), 3) New findings of cardiomyopathy on echocardiogram |
Countries
United States
Contacts
Primary ContactAnna L Huguenard, MD
Outcome results
None listed