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PubMed · 11988249

Effect of MRI noise on cochlear function.

P Radomskij·M A Schmidt·C W Heron·D Prasher
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Abstract

A disadvantage of magnetic resonance imaging (MRI) is the high level of noise produced (peaking between 122 dB and 131 dB). We used otoacoustic emissions (OAEs) as a method to quantify the effect of MRI-generated noise on the cochlea. OAEs were measured in 16 patients before and after MRI and in 16 controls. OAEs decreased in patients after MRI, but the controls, who were not exposed to MRI noise, showed no decrease over the same period. The change in OAEs shows a clear effect of MRI noise on cochlear function, despite use of earplugs. The importance of correctly fitted earplugs cannot be underestimated.

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CochleaCochlear DiseasesDeafnessHumansMagnetic Resonance ImagingOtoacoustic Emissions, SpontaneousRisk FactorsComparative StudyJournal ArticleResearch Support, Non-U.S. Gov't

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P Radomskij, M A Schmidt, C W Heron, D Prasher. 2002-04-27. Effect of MRI noise on cochlear function.. https://doi.org/10.1016/s0140-6736(02)08423-4

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The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing impairment are hair cell loss, signal transduction disturbances in the region of the outer and inner hair cells and the spiral ganglion, impairment of cochlear blood flow, mechanical disturbance, and hypoxia and ischemia. The present model surveys the possible cellular and molecular biological causes of peripherally developing hearing loss and tinnitus. In particular, the paper discusses the roles of hypoxia and ischemia in the cochlea and in the etiology of the neurosensory types of tinnitus. Peripheral origins of hearing disturbances and tinnitus may be: (a) damage to the stereocilia and the tip links, (b) dysfunction of potassium channels or (c) modification of the glutamate release. Moreover, the hypoxia inducible factor-1 may have an important role to play as a key transcription factor in the cells' adaptation to hypoxia and ischemia. An impairment of the cochlear blood flow may be induced by the expression of target genes like nitrogen monoxide synthase and endothelin-1 resulting in tinnitus. The paper discusses consequences resulting from the present model for the medical treatment of peripherally developing tinnitus and hearing loss.

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