Bilateral vestibulopathy (BVP)

The condition for which the rotational chair was originally built. If caloric responses are absent, you cannot tell whether the irrigation simply failed — but the chair can.

Clinical picture

BVP presents with chronic unsteadiness, gait ataxia worse in the dark or on uneven surfaces, and — most distinctive — oscillopsia: the visual world appearing to bounce during head movements. There is typically no spontaneous nystagmus, in contrast to acute unilateral lesions Hain TC 2013.

Pathophysiology

The condition is heterogeneous. Aminoglycoside vestibulotoxicity (especially gentamicin) is the commonest identifiable cause; others include meningitis, bilateral Ménière's disease, DFNA9 and other genetic disorders (e.g., the CANVAS syndrome — cerebellar ataxia, neuropathy and vestibular areflexia), and autoimmune inner-ear disease. A substantial fraction is idiopathic.

RCT pattern

On SHA, gain is symmetrically reduced across all frequencies, often below 0.2 throughout the band. Phase lead is elevated at every frequency (most dramatic at low frequencies). Symmetry is preserved — both ears are equally weak. The step-test Tc collapses toward the cupula value of ~5 s, reflecting loss of peripheral drive to velocity storage.

Diagnosis & differential

BVP is a clinical-physiological diagnosis: history and confirmatory testing on RCT, vHIT or caloric. The chair is the gold standard for low- and mid-frequency loss and is the test of choice when caloric responses are absent and the technical adequacy of irrigation is in doubt Strupp M 2017.

• Always ask about prior aminoglycoside exposure.
• Check for cerebellar signs and peripheral neuropathy — CANVAS is a treatable diagnosis to consider.
• Audiometry — bilateral hearing loss with vestibular loss raises Usher syndrome and DFNA9.