BMJ  2007;335:952 (10 November), doi:10.1136/bmj.39388.451019.1F

Letters

Aminoglycoside ototoxicity

Vestibular function is also vulnerable

The first 150 words of the full text of this article appear below.

We are concerned to correct a common misconception—namely, that ototoxicity is synonymous with deafness. Except for the rare cases of mitochondrial mutations discussed by Bitner-Glindzicz and Rahman, vestibular function is much more sensitive to aminoglycosides than hearing function.¹ Ninety per cent of patients with gentamicin associated vestibular loss will not be deaf.²

Most cases of aminoglycoside vestibulotoxicity with preserved hearing will not be diagnosed.³ The typical patient with aminoglycoside vestibular failure will have been in critical care often with renal failure. If not sedated, 20% experience spontaneous episodic vertigo² for a few days, with episodes lasting minutes to hours; an unexplained phenomenon as simultaneous, bilateral vestibular loss should not cause vertigo (since vertigo implies a right-left vestibular imbalance). The vertiginous episodes wane after a few days as the vestibular function is ablated. In all patients with aminoglycoside vestibulotoxicity, however, attempts to rehabilitate and mobilise are severely compromised due to gait . . . [Full text of this article]

Neuro-otology Unit, Department of Clinical Neuroscience, Imperial College, Charing Cross Hospital, London W6 8RF

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Relevant Article

Ototoxicity caused by aminoglycosides

Maria Bitner-Glindzicz and Shamima Rahman
BMJ 2007 335: 784-785. [Extract] [Full Text] [PDF]

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• Seemungal, B M, Bronstein, A M (2008). A practical approach to acute vertigo. PN 8: 211-221 [Abstract] [Full text]