Subclinical cochlear dysfunction in newly diagnosed relapsing-remitting multiple sclerosis

Background: Hearing impairment in multiple sclerosis has long been considered a process mainly related to the central auditory system. However, increasing evidence also suggests a peripheral involvement of the inner ear. The objective of this study was to investigate subclinical cochlear dysfunction and possible correlation with disease severity in untreated newly diagnosed multiple sclerosis patients using transient-evoked and distortion-product otoacoustic emissions.Methods: Forty patients with newly diagnosed relapsing-remitting multiple sclerosis, clinically normal hearing and no brainstem lesions (study group) and forty matched controls (control group) were included in the study. All subjects had a routine audiological evaluation including history and clinical examination, pure tone audiometry, acoustic immittance test, auditory brainstem response and otoacoustic emissions recording. Self-administered questionnaires were used to evaluate self-perception of hearing disability.Results: Auditory brainstem response and pure tone audiometry thresholds resulted within normal range in all patients. The amplitudes of transient-evoked and distortion-product otoacoustic emissions responses were significantly reduced at 1000, 1500, 2000 and 3000 Hz in the study group compared to the control group.Conclusions: This study shows decreased otoacoustic emission amplitudes in untreated multiple sclerosis patients with clinically normal hearing and no brainstem demyelinating plaques, suggesting a subclinical cochlear impairment. This alteration may represent an early sign of peripheral hearing damage, suggesting a role for otoacoustic emissions in the early diagnosis of cochlear dysfunction in multiple sclerosis patients. However, given that otoacoustic emissions primarily reflects cochlear function, and that the wave I of the auditory brainstem responses was spared, the evidence supporting a peripheral involvement of acoustic pathways due to multiple sclerosis can only be hypothetically attributed to an early subclinical involvement of outer hair cells.