The used round window approach for electrode insertion should be preferred to decrease the risk of loss of vestibular function and the occurrence of vertigo.

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Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). Unexposed animals were used as controls (n = 7). Frequency-specific auditory brainstem responses (ABR) were recorded to examine auditory thresholds. Cell density was determined within the dorsal (DCN) and ventral (VCN) cochlear nucleus; the central nucleus of the inferior colliculus (ICC); the dorsal, ventral, and medial subdivisions of the medial geniculate body (MGBd, MGBv, and MGBm); and layer I to VI of the primary auditory cortex (AI I-VI). ABR thresholds were significantly elevated in the TTS group (52-69 dB SPL) and in the PTS group (33-42 dB SPL) compared to controls. There was a significant decrease in cell density only in the VCN of the TTS group (-10%), most likely induced by the acute overstimulation of neurons. Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.

Minor trauma of the head, neck, and craniocervical junction can have major impact on the vestibular system at different sites. Patients need to be carefully diagnosed, even if the onset of vertigo occurs a few weeks or months after the initial trauma.

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The objective of this study was to investigate the occurrence of vestibular receptor deficiency and taste disorders after bilateral cochlear implantation in postlingually deafened patients and to find out whether the risk for these complications is higher for the second implantation. In a retrospective cohort study, we examined 20 patients (11-58 years, mean age 41.5 years), implanted sequentially between 2000 and 2007 (mean period between cochlear implantation 32.9 ± 25 months). Pre- and postoperative vestibular testing was performed by subjective rating [Dizziness Handicap Inventory (DHI)], caloric irrigation [vestibuloocular reflex (VOR)] and by vestibular-evoked myogenic potential (VEMP) recordings for saccular function. The sense of taste was evaluated pre- and postoperatively by a questionnaire and testing (sour/sweet/bitter/salty bilaterally on the tongue). DHI evaluation showed a moderate not significant mean increase by 2.7 ± 7.7 SD points after the first and a significant increase by 9.4 ± 16.6 SD points after the second implantation. Ipsilateral VEMP responses disappeared in three ears (27.3%) after the first and in two ears (18.2%) after the second operation. VOR disappeared only once (5.9%) after the first implantation. One (5%) patient complained of a persisting disturbance of taste in the questionnaire after unilateral and 3 (15%) after bilateral implantation. Specific testing showed in one case (5%) a unilateral taste disorder after ipsilateral cochlear implantation. Our data show that there is a higher risk for subjective vertigo after the second implantation. The occurrence of unilateral and/or bilateral vestibular dysfunction and the potential risk of taste disorder should be included in the risk counseling before bilateral cochlear implantation to increase patients' and medicolegal safety in the decision-making process.

Cochlear implant surgery has become a successful procedure for deaf patients to restore their hearing again. Some of the patients, however, complain of persisting dizziness after the surgery which can have a major impact on their quality of life. Neurotological tests of the vestibular system were applied in a total of 18 cochlear implantees pre- and postoperatively. In addition, vestibular evoked myogenic potentials were evoked intraoperatively to investigate possible interferences of the electrically stimulated cochlear implant electrode (eVEMP) with vestibular receptor cells of the saccule in more detail. After cochlear implantation, the saccular function was impaired in the majority of the patients. However, eVEMPs could be recorded intraoperatively in all patients by intracochlear, high-level electrical stimulation via the cochlear implant electrode. In essence, acute, short-term dizziness after cochlear implantation seems to result primarily from a transient vestibular deficit of various origins. In contrast to this, chronic, persisting dizziness after cochlear implant surgery is largely based on a dysfunction of the saccular macula which is an integral component of the otolith system. This saccular impairment is induced most likely by the insertion trauma of the cochlear implant electrode when advancing it into the inner ear. A possible coactivation of the inferior vestibular nerve by the electrical stimulation might play an additional role in the pathogenesis of the persisting postsurgical dizziness.