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We report enhanced symmetrical cervical vestibular evoked myogenic potential (cVEMP) but asymmetrical ocular VEMP (oVEMP) responses in a patient with CT-verified bilateral superior semicircular canal dehiscence (SCD) but with acute vestibular syndrome. This implies that absence of unilateral utricular macula function alone is sufficient to cause symptoms of acute vertigo. Acute vertigo should not automatically be presumed to originate from semicircular canal dysfunction.To identify the cause of an acute vertigo attack in a patient with bilateral SCD.The functional state of all peripheral vestibular sense organs was tested using the video head impulse test (vHIT) for all semicircular canals and VEMPs to air-conducted sound (ACS) or bone-conducted vibration (BCV) to test all otolith organs. The cVEMP tested mainly saccular function and the oVEMP mainly utricular function.All semicircular canals showed normal function. The cVEMPs showed enhanced, but symmetrical saccular function. In contrast, oVEMPs showed an enhanced but asymmetric n10 component - it was greatly reduced beneath the left eye, implying decreased function in the right utricular macula. That result was confirmed using very high frequency stimuli which are effective in SCD: 4000 Hz BCV stimuli showed that oVEMP n10 was present beneath the right eye but absent beneath the left eye.

To measure horizontal semicircular canal function over days, weeks, and months after an acute attack of vestibular neuritis.The video head impulse test (vHIT) was used to measure the eye movement response to small unpredictable passive head turns at intervals after the attack.Two patients diagnosed with acute right unilateral vestibular neuritis.There was full restoration of horizontal canal function in one patient (A) as shown by the return of the slow phase eye velocity response to unpredictable head turns, while in the other patient (B) there was little or no recovery of horizontal canal function. Instead this second patient generated covert saccades during head turns.Despite the objective evidence of their very different recovery patterns, both patients reported, at the final test, being happy and feeling well recovered, even though in one of the patients there was clear absence of horizontal canal function. The results indicate covert saccades seem a successful way of compensating for loss of horizontal canal function after unilateral vestibular neuritis. Factors other than recovery of the slow phase eye velocity are significant for patient recovery.

The enhanced sound- and vibration-induced vestibular evoked myogenic potentials (VEMPs) and their lower threshold in patients with a thinning of the bony wall of the superior semicircular canal (superior canal dehiscence, SCD) have been interpreted as being due to the dehiscence allowing sound and vibration to activate, unusually, the receptors of the dehiscent semicircular canal. We report a patient with bilateral SCD, as verified by high resolution CT scans, who had bilaterally decreased superior semicircular canal function, as shown by rotational tests of canal function. This patient also showed enhanced VEMPs and reduced thresholds. We conclude that in this patient the enhanced VEMP responses are thus probably due to enhanced otolithic stimulation by sound and vibration after dehiscence.