Bilateral vestibulopathy

The author explains the clinical presentation, pathophysiology, prevention, diagnostic work-up, and management of bilateral vestibulopathy. Gait ataxia and oscillopsia are the key clinical features of bilateral vestibulopathy. Other clinical features of bilateral vestibulopathy include absence of spontaneous vertigo and nystagmus; inability to walk in the dark or on uneven or soft surfaces, unless by holding on to the wall or objects in the room (ie, use of contact cues); Romberg sign; no dysmetria or dysdiadochokinesis; insensitivity to motion sickness; a bilateral, usually symmetric, decreased sensitivity to caloric and rotational stimulation; and decreased or absent ocular counter-rolling. The most common causes of bilateral vestibulopathy are ototoxic aminoglycosides, Ménière disease, and meningitis. Clinicians should be particularly aware of risk factors for aminoglycoside-induced ototoxicity, including family history of ototoxicity, high serum levels, higher total dose, longer duration of therapy (beyond 7 to 10 days), intrathecal administration, previous exposure to ototoxins, concomitant use of other nephrotoxic or ototoxic drugs, renal impairment, fever, and older age. An imperceptible level of galvanic vestibular stimulation, delivered as “zero-mean current noise” (so-called “noisy galvanic vestibular stimulation”), may be effective in improving postural stability in patients with bilateral vestibular dysfunction.