Abstract: Migraine is a neurological disease characterized by the sensitization of trigeminal nociceptive neurons. The association and pathophysiology between migraine and auditory manifestations remain conflicting. This study aims to identify the risk of accompanying hyperacusis, sudden hearing loss, and brainstem dysfunction in patients with migraines. The results revealed no changes in hearing, significant hyperacusis, and elevated contralateral acoustic reflex thresholds during a migraine attack in participants with episodic and chronic migraines, compared to their baseline and to the control group. The data from both migraine groups support the presence of central gain and brainstem dysfunction.
Summary:
Rationale/
Purpose: Migraine is a common neurological disorder that affects 12% of the population. Neuroanatomical data indicates that trigeminal pathway and auditory information converge and evoke responses in auditory neurons. Both auditory and vestibular manifestations are reported among migraine patients. However, research mainly focused on vestibular migraine, with little attention has been given to auditory manifestations. The reported association between migraine and auditory manifestations remains conflicting due to poorly defined migraine participants and study design. This study aims to identify the risk of accompanying hyperacusis, sudden hearing loss, cochlear dysfunction, and brainstem function during migraine attacks in patients with episodic and chronic migraines. It was hypothesized that migraine causes both peripheral and central brainstem changes during the migraine attack compared to the non-migraine group.
Methods: Participants included a total of 30 normal-hearing individuals in the age range of 18-45. Twenty of them with a clinical diagnosis of migraine (10 episodic and 10 chronic) and 10 matched individuals with no migraine of any type (control group). All participants were tested using a questionnaire, pure-tone audiometry at conventional and extended high frequencies, speech audiometry in quiet and in noise, uncomfortable loudness levels (ULL), distortion-product otoacoustic emission (DPOAE), and acoustic reflex thresholds (ART). The two experimental migraine groups were tested twice at baseline and then during a migraine attack, and the control group was also tested twice at baseline and then within a month. Results from both ears were compared between the three groups and between the two test visits using mixed model repeated measures analysis of variance measures.
Results &
Conclusions: At baseline, all participants exhibited normal hearing thresholds (≤25 dB HL) at both conventional and extended high frequencies. They achieved excellent word recognition and within normal QuickSIN scores. DPOAEs were present (≥ 6 dB signal-noise-ratio), and acoustic reflex thresholds were within the normal range (≤ 100 dB HL), with no statistically significant differences between groups (p > 0.05). However, baseline ULL values at all tested frequencies were significantly lower for both migraine groups (ranging from 80 to 65 dB HL) compared to the control group (ULL values > 90-100 dB HL).
During the migraine attack, there were no statistically significant changes in hearing thresholds, word recognition scores in quiet, or DPOAEs in migraineurs and the control group. The ULL values significantly decreased to a range of 65-40 dB HL (p < 0.001) in the chronic migraine group, and the QuickSIN scores showed mild-to-moderate signal-to-noise ratio loss and the contralateral acoustic reflex thresholds were elevated in both migraine groups compared to their baseline and compared to the control group.
In conclusion, there were no signs of sudden hearing loss or cochlear dysfunction during migraine attacks in both the episodic and chronic migraine groups. However, migraineurs experienced severe hyperacusis and had difficulty hearing speech in background noise. Additionally, they exhibited bilaterally elevated contralateral acoustic reflex thresholds during migraine attacks. These findings support the hypothesis that migraine, episodic and chronic, results in central gain and potential dysfunction at the brainstem level, particularly within the superior olivary complex.
Learning Objectives:
Discuss the differences between different types of noise sensitivity.
Define migraine and the trigeminal nociceptor pathway.
Explain the main findings of episodic and chronic migraine on the auditory system.
