Transcutaneous Auricular Vagus Nerve Stimulation for Misophonia

A 64-year-old woman with severe misophonia, triggered specifically by the sound of a basketball bouncing, saw her symptom severity score drop from 80 to 9 after a one-month experimental treatment. The intervention, bilateral transcutaneous auricular vagus nerve stimulation (taVNS), targeted the autonomic nervous system dysregulation often central to the condition. According to a new case report by Francesca Proietti, Massimo Marano, and Emanuele Rizzo, the patient’s improvement was substantial and sustained at a one-month follow-up.

## How Vagus Nerve Stimulation Targets Misophonia’s Physical Fury

Misophonia is more than an aversion to sound. For those affected, specific “trigger” sounds—like chewing, sniffing, or, in this case, a bouncing basketball—can provoke an immediate, intense fight-or-flight response. This includes emotional rage or panic, but also pronounced physical symptoms: heart palpitations, shortness of breath, sweating, and a choking sensation. Researchers Proietti, Marano, and Rizzo hypothesized that this autonomic nervous system hyperarousal could be a key treatment target.

Their chosen method was transcutaneous auricular vagus nerve stimulation. This non-invasive technique involves placing small electrodes on the outer ear to deliver a mild electrical current. This current activates branches of the vagus nerve, a major nerve pathway that helps regulate the body’s stress response, heart rate, and mood. The goal was to use this stimulation to “calm” the exaggerated autonomic reaction to trigger sounds. The patient received stable-dose sertraline (an SSRI) throughout the study, with taVNS as an add-on intervention.

## Treatment Protocol and Immediate Outcomes

The patient underwent a one-month protocol of daily, 60-minute bilateral taVNS sessions. The stimulation intensity was individually adjusted to a level that was strong enough to be felt but not painful. To measure impact, the team used the Duke Misophonia Questionnaire Symptoms Composite Scale, where higher scores indicate greater severity.

The change was pronounced. The patient’s score fell from a baseline of 80 to 9 immediately after the treatment period. At the one-month follow-up assessment, it had dropped further to 5. This indicates a near-total remission of the core misophonic reactivity that was sustained after treatment stopped. The report also notes that other measures of psychological distress, including anxiety, hostility, and depressive symptoms, improved alongside the primary misophonia measure.

## A Complex Picture: Symptoms vs. Function

While the reduction in symptom severity was clear and persistent, two other outcome measures painted a more nuanced picture. First, the patient’s sleep quality improved after the month of taVNS but had returned to baseline levels by the follow-up visit. This suggests that any sleep benefit may require ongoing treatment.

Second, and more notably, the patient’s self-reported functional impairment—how much misophonia interfered with her daily life—decreased right after treatment but had increased again by follow-up, even though her symptom severity score remained very low. The authors propose this reveals a “dissociation between symptom reduction and perceived functional recovery.” In practical terms, even though the physical and emotional reaction to the trigger sound was vastly diminished, the patient’s long-standing patterns of avoidance and distress in anticipation of triggers may have taken longer to unwind. This highlights that effective misophonia management might require both biological interventions to lower reactivity and psychological strategies to address behavioral impacts. For readers interested in psychological approaches, our article on cognitive reappraisal for misophonia explores one such method.

## Implications and the Need for Rigorous Study

This single case report, detailed in the journal *Frontiers in Psychology* (DOI: 10.3389/fpsyg.2026.1903444), offers a promising but preliminary proof of concept. It directly supports the growing theory that misophonia involves dysfunctional connections between the auditory and limbic systems, leading to autonomic storm. The findings suggest that non-invasive neuromodulation aimed at the vagus nerve could be a feasible adjunctive therapy for individuals, particularly those with prominent physical arousal symptoms.

The authors are careful to state their results are hypothesis-generating. A single case cannot prove efficacy. The observed benefits could be influenced by the placebo effect, or by the concurrent stable use of sertraline. The dissociation between symptom scores and functional impairment also calls for a more holistic view of treatment success. As research into the brain mechanisms of hearing disorders advances, it may help identify which patients are most likely to benefit from neuromodulation.

Future research must involve randomized, sham-controlled clinical trials with larger groups of participants. Such studies can isolate the specific effect of taVNS from other factors and help clarify optimal treatment protocols. For now, this case adds a new, physiological option to the very short list of potential misophonia interventions and provides a clear direction for future investigation. If you are interested in other neuromodulation approaches for auditory conditions, you can read about prior research on taVNS for misophonia. Furthermore, the observed fluctuation in sleep quality underscores that managing co-occurring symptoms is complex; resources like an evidence-based sleep hygiene guide may provide useful general support.