Background

Bilateral vestibular loss is characterised by symmetrically reduced or absent vestibular function in both inner ears. Patients typically complain of unsteadiness that worsens in darkness or on uneven ground, and oscillopsia, a sensation that the visual world bounces during head movement. This case report describes the second patient in a series of individuals presenting with a progressive form of bilateral vestibular impairment of unknown cause.

Case Presentation

A man in his late sixties presented with a two-year history of gradually worsening imbalance. He reported feeling particularly unstable while walking in dimly lit environments and when turning quickly. He also described blurred vision when walking or riding in a vehicle, consistent with oscillopsia. He denied vertigo, hearing loss, tinnitus, or aural fullness. There was no history of meningitis, ototoxic drug exposure, head trauma, or autoimmune disease. He had no family history of balance disorders.

Examination

Gait was cautious with a slightly widened base. He could stand with feet together with eyes open without difficulty, but sway increased markedly with eye closure. Romberg testing was positive. He had normal eye movements, with no spontaneous or gaze-evoked nystagmus. Head impulse testing to the left and right revealed obvious corrective saccades, suggesting bilaterally impaired vestibulo-ocular reflexes. The remainder of the neurological examination, including cerebellar testing and sensory examination of the lower limbs, was normal.

Investigations

Audiometry showed age-appropriate hearing bilaterally. Video head impulse testing confirmed reduced gains for all six semicircular canals, more prominent for the horizontal canals. Caloric testing revealed no response to ice-water irrigation in either ear, indicating severe loss of lateral canal function. Dynamic visual acuity testing demonstrated a loss of more than four lines of visual acuity with head movement. Magnetic resonance imaging of the internal auditory meatus and brain showed no structural abnormality. Serological testing for inflammatory or autoimmune markers was unremarkable.

Differential Diagnosis

Progressive bilateral vestibular loss may result from ototoxicity, meningitic infection, bilateral Meniere disease, autoimmune inner ear disease, or neurodegenerative conditions. In this patient, the absence of relevant drug exposure, infection history, hearing involvement, and inflammatory markers made these causes less likely. A slowly progressive, isolated bilateral vestibulopathy without additional neurological features may represent an idiopathic or possibly degenerative disorder restricted to the vestibular end organs or the vestibular nerve.

Management and Outcome

The patient was referred for specialised vestibular rehabilitation. The programme focused on gaze stabilisation exercises, balance training on compliant surfaces, and habituation exercises to reduce reliance on visual cues. He was advised to use a walking stick at night and to avoid tasks that required simultaneous head and body rotation. Over six months, he reported improved confidence and a modest reduction in oscillopsia, although objective vestibular function remained unchanged. He was counselled about fall prevention and safety strategies for locomotion.

Discussion

This case illustrates the typical presentation of progressive bilateral vestibular loss without auditory features. The combination of oscillopsia, gait unsteadiness aggravated by eye closure, bilaterally abnormal head impulse responses, and absent caloric responses is diagnostic. Vestibular rehabilitation remains the mainstay of management, focusing on compensation rather than restoration of peripheral function. Clinicians should consider this diagnosis in older adults presenting with unexplained imbalance and visual distortion during movement.

Conclusion

Progressive bilateral vestibular loss should be recognised as a distinct clinical entity within the spectrum of balance disorders. Early identification allows for timely rehabilitation and fall prevention strategies. Further research is needed to clarify whether such cases represent an autoimmune, degenerative, or otherwise distinct pathological process.