Migraine and Hearing Disorders: A Shared Link

A systemic disorder of multisensory sensitization, migraine affects the auditory system in up to 49% of patients. A comprehensive 2026 review in the *Journal of Neurology* synthesizes the evidence, moving beyond simple comorbidity to propose a clear mechanistic model for why migraine is a significant driver of hearing loss, tinnitus, and hyperacusis.

Epidemiology and Audiological Evidence

The research team, led by Xu, Zhai, and Chen, analyzed a wide body of existing literature. Their findings show the auditory burden of migraine is both common and measurable. Epidemiological data indicates that between 15% and 49% of individuals with migraine report co-occurring auditory symptoms. These are not just subjective complaints; objective audiological assessments reveal that nearly two-thirds (approximately 65%) of migraine patients exhibit abnormalities in auditory electrophysiological tests. These tests can detect issues like impaired efferent auditory pathway function or signs of hidden hearing loss that standard audiograms might miss. This high rate of objective abnormality confirms that migraine-related auditory dysfunction is a real physiological phenomenon, not merely a perceptual overlap.

The Three-Axis Pathophysiological Model

The review’s central contribution is framing the problem as a “peripheral-to-central continuum” driven by three interacting pathological axes. This model explains how a brain disorder like migraine can directly damage the delicate inner ear and alter central sound processing.

Axis 1: Vascular and Hydrodynamic Vulnerabilities

The first axis involves anatomy and fluid dynamics. The inner ear’s blood supply is fragile and terminal, making it highly susceptible to the microvascular ischemia and blood flow dysregulation common during migraine attacks. Furthermore, the researchers point to potential aberrations in brain-ear fluid exchange. This could mean that chemical or pressure changes in the cerebrospinal fluid, influenced by migraine, directly disrupt the perilymph and endolymph of the cochlea, its functional environment.

Axis 2: Local Neurochemical Imbalance

Within the cochlea itself, migraine processes create a toxic local environment. The review details a cascade involving glutamate excitotoxicity, abnormal neuropeptide signaling (like that of calcitonin gene-related peptide, CGRP, a key migraine mediator), and activation of the innate immune system. Together, these factors disrupt the precise ionic balance and cellular homeostasis required for healthy hair cell function and neuronal signaling, potentially leading to sensorineural damage. This local damage aligns with research into otoactive compounds and targets that aim to protect this microenvironment.

Axis 3: Central Sensitization and Network Dysfunction

The third axis operates in the brain. Migraine is characterized by central sensitization—a state where the nervous system becomes hyper-responsive. In the auditory domain, this manifests as impaired efferent gating (the brain’s ability to filter out irrelevant sounds) and thalamocortical dysrhythmia. This is a dysfunctional rhythm between the thalamus and auditory cortex that is strongly implicated in the generation of tinnitus and hyperacusis. This central component explains why auditory symptoms can persist between migraine headaches and why conditions like misophonia may be more prevalent. Understanding this central hypersensitivity is a focus of approaches like cervical stimulation and neuromodulation.

Clinical Implications and Future Directions

The authors state that clinical management remains suboptimal due to fragmented understanding, variable audiological assessment protocols, and scattered data on treatment efficacy. Their three-axis model directly informs a new framework for developing therapies based on specific clinical objectives.

Strategies are now being categorized by their target: 1) blocking upstream migraine pathways (e.g., with CGRP monoclonal antibodies), 2) protecting the cochlear microenvironment (using antioxidants or anti-excitotoxic agents), and 3) correcting central hypersensitivity (through neuromodulation or behavioral therapies). This precision approach could move care beyond generic sound therapy or migraine prophylaxis. For instance, the drive to protect the inner ear microenvironment is closely related to advances in nanocarriers for otic drug delivery, which aim to deliver protective agents directly to the cochlea.

The framework calls for more translational research to validate these links, promote early identification of auditory phenotypes in migraine patients, and establish cross-disciplinary management between neurologists and otologists. For patients, this means the increasing recognition of their auditory symptoms as a core part of their migraine disorder, not an unrelated coincidence, which should lead to more comprehensive and effective treatment strategies in the future.

Source: Xu W, Zhai N, Chen J, et al. Migraine and auditory dysfunction: beyond comorbidity. J Neurol. 2026;273(7):433. doi:10.1007/s00415-026-13957-0.