ReviewJournal of neurology2026
Migraine and auditory dysfunction: beyond comorbidity.
Review in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.