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Aviat Space Environ Med. 2012 Nov;83(11):1097-100.

Superior vestibular dysfunction in severe decompression sickness suggests an embolic mechanism.

Author information

  • 1Department of Audiology and Neurotology, Karolinska University Hospital, Stockholm, Sweden. luca.verrecchia@karolinska.se

Abstract

BACKGROUND:

Both nitrogen bubble embolism and the difficulty of inner ear tissues to wash out nitrogen have been discussed as possible reasons for the selective vulnerability of the inner ear to decompression illness. This case report suggests that nitrogen bubble embolism plays a crucial role in the pathogenesis of inner ear lesions in decompression accidents.

CASE REPORT:

The current patient, a 48-yr-old male dive master, suffered a severe decompression illness with vertigo as the only residual symptom. At the 1-mo follow-up, neuro-otological evaluation revealed a selective lesion of the superior vestibular division of the left labyrinth with normal functioning inferior vestibular division. At vestibular testing, there was no caloric response from the affected left ear, and the head impulse tests for the lateral and anterior semicircular canal were also impaired. Tests of vestibular evoked myogenic potentials (VEMP) showed divergent results. Ocular VEMP in response to left ear stimulation were absent, whereas the cervical VEMP were completely symmetrical and normal. Thus, the lesion profile implies a partial vestibular loss selectively affecting the superior vestibular division of the inner ear.

DISCUSSION:

The most likely explanation for such a selective injury seems to be bubble microembolism coupled with both the specific anatomy of this terminally supplied subunit, and with the slow nitrogen wash-out of the vestibular organ.

PMID:
23156099
[PubMed - indexed for MEDLINE]
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