Key Findings
Migraine operates as a systemic disorder of multisensory sensitization. Within this spectrum, auditory manifestations, including sensorineural hearing loss, tinnitus, and hyperacusis, represent prevalent yet frequently overlooked otologic phenotypes. Epidemiological data show that 15%-49% of migraine patients present with comorbid auditory symptoms, and nearly two-thirds exhibit auditory electrophysiological abnormalities. However, optimal clinical management remains constrained by an incomplete understanding of pathogenic mechanisms, variable audiological assessment protocols, and dispersed therapeutic data. This review synthesizes epidemiological, audiological, and pathophysiological data linking migraine to auditory dysfunction. The underlying pathology involves a peripheral-to-central continuum across three interacting axes. Anatomical and hydrodynamic vulnerabilities drive localized microvascular ischemia and aberrant brain-ear fluid exchange. Localized neurochemical imbalances, involving glutamate excitotoxicity, neuropeptide signaling, and innate immune activation, disrupt inner ear homeostasis. Concurrently, central sensitization facilitates neural network plasticity, characterized by impaired efferent gating and thalamocortical dysrhythmia. Drawing upon these underlying pathways, current and emerging therapeutic strategies are categorized by specific clinical objectives: blocking upstream migraine pathways, protecting the cochlear microenvironment, and correcting central hypersensitivity. This framework aims to catalyze future translational research to rigorously validate these mechanistic links, promote early identification, precise clinical phenotyping, and cross-disciplinary management of affected patients.
Why This Matters for Body-Mind Practice
[Draft — editorial context needed]
Source
- Migraine and auditory dysfunction: beyond comorbidity. — Journal of neurology
