Migraine and Hearing Disorders Explained

Migraine operates as a systemic disorder of multisensory sensitization, and auditory symptoms are a core part of its clinical picture. A 2026 review in the *Journal of Neurology* synthesizes evidence that hearing loss, tinnitus, and hyperacusis are not just occasional companions to migraine but are prevalent otologic phenotypes driven by shared pathology. The analysis, led by researchers Xu, Zhai, and Chen, details a “peripheral-to-central continuum” of dysfunction and proposes a structured treatment framework based on these mechanisms.

Migraine’s Auditory Burden: A Common but Overlooked Link

The epidemiological data presented by Xu and colleagues is striking. They report that 15% to 49% of individuals with migraine present with comorbid auditory symptoms. These are not minor complaints; the spectrum includes sensorineural hearing loss, tinnitus (ringing in the ears), and hyperacusis (reduced tolerance to sound). Perhaps more revealing is the finding that nearly two-thirds of migraine patients exhibit abnormalities on auditory electrophysiological tests. This suggests underlying auditory system dysfunction is widespread, even in patients who may not yet report specific hearing issues. The authors argue these manifestations are frequently overlooked in clinical practice, leaving a significant portion of the patient’s sensory experience unaddressed.

A Three-Axis Pathophysiological Model

The core of the review proposes a unified model explaining how migraine leads to auditory dysfunction. The pathology unfolds across three interacting axes, creating a “peripheral-to-central continuum.”

The first axis involves anatomical and hydrodynamic vulnerabilities. Specific structures in the inner ear and its vascular supply may be predisposed to microvascular ischemia (reduced blood flow) and aberrant fluid exchange during migraine events. This creates a fragile local environment.

The second axis is localized neurochemical imbalance. Within the inner ear, migraine-related processes like glutamate excitotoxicity, abnormal neuropeptide signaling (e.g., CGRP), and innate immune activation can directly disrupt cochlear homeostasis. This is akin to a migraine happening in the miniature, sensitive world of the inner ear.

The third and integrating axis is central sensitization. This is a state of hyper-responsiveness in the central nervous system. The review describes how this facilitates maladaptive neural plasticity, specifically impairing the brain’s efferent (descending) ability to “gate” or filter auditory signals and promoting thalamocortical dysrhythmia. This axis directly links to conditions like hyperacusis and tinnitus, where the brain’s interpretation of sound becomes distorted. This model of central hypersensitivity shares conceptual ground with mechanisms proposed for other sound tolerance disorders, such as the role of emotional regulation in misophonia.

From Mechanism to a Structured Treatment Framework

Moving beyond simply noting a correlation, the authors use their three-axis model to categorize current and emerging therapeutic strategies by specific clinical objective. This creates a more rational approach to management.

1. Blocking Upstream Migraine Pathways

This strategy aims to prevent the entire cascade. It includes established migraine preventatives and newer agents like CGRP monoclonal antibodies. By calming the systemic disorder, the theory is that the triggers for cochlear ischemia and neurochemical storms are reduced.

2. Protecting the Cochlear Microenvironment

Targeted at the first two axes, this objective focuses on local protection. Strategies could include antioxidants to combat excitotoxicity, anti-inflammatory agents, or treatments aimed at stabilizing inner ear fluid dynamics. Research into localized delivery, such as via nanocarriers for otic delivery, is directly relevant to this goal.

3. Correcting Central Hypersensitivity

For symptoms rooted in the brain’s processing, treatments aim to retrain neural networks. This includes sound therapy, cognitive behavioral therapy (CBT), and neuromodulation approaches. The effectiveness of combining CBT and sound therapy for tinnitus finds a clear rationale here. Furthermore, techniques like cervical stimulation, which may influence central auditory pathways, fit into this category. The process of correcting central hypersensitivity shares therapeutic principles with interventions for other conditions involving maladaptive brain states, such as the approach described in research on CBT-I outcomes for insomnia.

Practical Implications for Patients and Clinicians

For individuals with migraine, this review underscores the importance of mentioning any auditory changes—ringing, fullness, sensitivity to sound, or hearing fluctuations—to their healthcare providers. These are not separate, unrelated issues but likely part of the migraine process itself. For clinicians, the findings argue for incorporating simple audiological screening or questioning into migraine assessments. Early identification can guide more comprehensive, cross-disciplinary management involving neurology and otology.

The framework proposed by Xu et al. (PMID: 42371148) moves the conversation from comorbidity to shared mechanism. It provides a roadmap for future research to validate specific treatments for each axis and for clinicians to think more systematically about the full sensory impact of migraine. Recognizing migraine as a disorder of multisensory sensitization is the first step toward better management of its often-distressing auditory symptoms.