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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 imbalance and disabling oscillopsia on head movement. Occasionally, vestibular sedatives (for example, stemetil) are administered, which further compromises balance. Some patients are labelled as having had a cerebellar stroke.
The diagnosis of vestibulotoxicity must be considered in patients with a history of aminoglycoside administration who develop head movement induced oscillopsia and gait imbalance. The diagnosis is easily made clinically via the head impulse test4 and confirmed by caloric testing. Aminoglycoside vestibular failure, which is permanent, can have devastating consequences for a patient's mobility and functional independence. Functional recovery, which is never complete, is slow (over years). Graded physical activity is important in aiding the recovery of gait and balance function.
Competing interests: None declared.