Migraine and auditory dysfunction: beyond comorbidity

Le résumé fourni par la source

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. A conceptual framework for the mechanism-driven assessment and targeted therapy of migraine-associated auditory dysfunction. This flowchart illustrates the phenotype-driven clinical management pathway for migraine-related otologic symptoms. The vertical axis delineates the theoretical pathophysiological continuum from peripheral structural vulnerability to central network dysregulation. Specific pathophysiological drivers (vascular and fluid dysregulation, neurochemical cascades, and maladaptive central plasticity) are hypothesized to manifest as distinct clinical phenotypes (solid black arrows). These auditory manifestations guide tiered audiological assessments to pinpoint precise functional deficits, ranging from occult cochlear vulnerability to sensory gating failures. Finally, mechanism-based targeted therapies are mapped to their corresponding pathophysiological origins (red dashed lines with inhibitory symbols), highlighting a multidisciplinary approach encompassing microenvironment protection, upstream neuropeptide blockade, and correction of central hypersensitivity.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.