To assess vestibular evoked myogenic potentials in patients with fibromyalgia syndrome.

Twenty-four patients with fibromyalgia syndrome (two men and 22 women) and 21 female controls were included in the study. All patients underwent vestibular evoked myogenic potential testing.

Statistical comparison of fibromyalgia patients with control subjects showed a significant difference with respect to n23 latencies and interpeak latencies (p < 0.05). There was no significant difference in p13 latencies, nor in p13 amplitudes, n23 amplitudes or interpeak amplitudes (p > 0.05).

Although patients with fibromyalgia syndrome generally have subjective neurotological symptoms, clinical and laboratory assessments usually fail to detect any objective abnormality. However, it is possible to detect abnormalities on vestibular evoked myogenic potential testing in such patients, indicating dysfunction in the vestibulospinal pathway, possibly in the saccule. Elongation of the n23 latency and of the interpeak latency of waves p13–n23, during vestibular evoked myogenic potential testing, may be a useful, objective indicator demonstrating neurotological involvement in fibromyalgia syndrome patients. Future research investigating the mechanisms of this latency elongation may help increase understanding of the pathogenesis of fibromyalgia syndrome.

To assess contralateral suppression of transiently evoked otoacoustic emissions in patients with fibromyalgia syndrome and normal hearing.

Twenty-four female patients with fibromyalgia syndrome and 24 healthy female controls with normal hearing were assessed using pure tone audiometry and transiently evoked otoacoustic emissions.

All patients with fibromyalgia syndrome and all controls had normal hearing on pure tone audiometry. In the patients with fibromyalgia syndrome, the mean transiently evoked otoacoustic emission amplitude was 15.5 ± 4.8 dB. The mean transiently evoked otoacoustic emission amplitudes after contralateral suppression was 15.5 ± 4.9 dB. There was no statistically significant difference between the transiently evoked otoacoustic emission amplitudes measured before and after contralateral suppression (p > 0.05). In the controls, the mean transiently evoked otoacoustic emission amplitude was 12 ± 5 dB. The mean transiently evoked otoacoustic emission amplitudes after contralateral suppression was 11 ± 4.7 dB. There was a statistically significant decrease in transiently evoked otoacoustic emission amplitudes after contralateral suppression (p < 0.01).

The mechanisms related to contralateral suppression of transiently evoked otoacoustic emissions seem dysfunctional in fibromyalgia syndrome. This dysfunction may be at the brain stem level, where the medial superior olivary complex is located, or at the synapses of medial superior olivary complex fibres with the outer hair cells in the cochlea. Demonstration of lack of contralateral suppression of transiently evoked otoacoustic emissions can be used as a diagnostic tool in patients with fibromyalgia syndrome.