Central Nervous Activity upon Systemic Salicylate Application in Animals with Kanamycin-Induced Hearing Loss--A Manganese-Enhanced MRI (MEMRI) Study.

This study investigated the effect of systemic salicylate on central auditory and non-auditory structures in mice. Since cochlear hair cells are known to be one major target of salicylate, cochlear effects were reduced by using kanamycin to remove or impair hair cells. Neuronal brain activity was measured using the non-invasive manganese-enhanced magnetic resonance imaging technique. For all brain structures investigated, calcium-related neuronal activity was increased following systemic application of a sodium salicylate solution: probably due to neuronal hyperactivity. In addition, it was shown that the central effect of salicylate was not limited to the auditory system. A general alteration of calcium-related activity was indicated by an increase in manganese accumulation in the preoptic area of the anterior hypothalamus, as well as in the amygdala. The present data suggest that salicylate-induced activity changes in the auditory system differ from those shown in studies of noise trauma. Since salicylate action is reversible, central pharmacological effects of salicylate compared to those of (permanent) noise-induced hearing impairment and tinnitus might induce different pathophysiologies. These should therefore, be treated as different causes with the same symptoms.

Bilateral Changes of Spontaneous Activity Within the Central Auditory Pathway Upon Chronic Unilateral Intracochlear Electrical Stimulation.

OBJECTIVES: In recent years, cochlear implants have been applied successfully for the treatment of unilateral hearing loss with quite surprising benefit. One reason for this successful treatment, including the relief from tinnitus, could be the normalization of spontaneous activity in the central auditory pathway because of the electrical stimulation. The present study, therefore, investigated at a cellular level, the effect of a unilateral chronic intracochlear stimulation on key structures of the central auditory pathway. DESIGN: Normal-hearing guinea pigs were mechanically single-sided deafened through a standard HiFocus1j electrode array (on a HiRes 90k cochlear implant) being inserted into the first turn of the cochlea. Four to five electrode contacts could be used for the stimulation. Six weeks after surgery, the speech processor (Auria) was fitted, based on tNRI values and mounted on the animal's back. The two experimental groups were stimulated 16 hours per day for 90 days, using a HiRes strategy based on different stimulation rates (low rate (275 pps/ch), high rate (5000 pps/ch)). The results were compared with those of unilateral deafened controls (implanted but not stimulated), as well as between the treatment groups. All animals experienced a standardized free field auditory environment. RESULTS: The low-rate group showed a significantly lower average spontaneous activity bilaterally in the dorsal cochlear nucleus and the medial geniculate body than the controls. However, there was no difference in the inferior colliculus and the primary auditory cortex. Spontaneous activity of the high-rate group was also reduced bilaterally in the dorsal cochlear nucleus and in the primary auditory cortex. No differences could be observed between the high-rate group and the controls in the contra-lateral inferior colliculus and medial geniculate body. The high-rate group showed bilaterally a higher activity in the CN and the MGB compared with the low-rate group, whereas in the IC and in the AC a trend for an opposite effect could be determined. CONCLUSIONS: Unilateral intracochlear electrical stimulation seems to facilitate the homeostasis of the network activity, since it decreases the spontaneous activity that is usually elevated upon deafferentiation. The electrical stimulation per se seems to be responsible for the bilateral changes described above, rather than the particular nature of the electrical stimulation (e.g., rate). The normalization effects of electrical stimulation found in the present study are of particular importance in cochlear implant recipients with single-sided deafness.

Acute and long-term effects of noise exposure on the neuronal spontaneous activity in cochlear nucleus and inferior colliculus brain slices.

Noise exposure leads to an immediate hearing loss and is followed by a long-lasting permanent threshold shift, accompanied by changes of cellular properties within the central auditory pathway. Electrophysiological recordings have demonstrated an upregulation of spontaneous neuronal activity. It is still discussed if the observed effects are related to changes of peripheral input or evoked within the central auditory system. The present study should describe the intrinsic temporal patterns of single-unit activity upon noise-induced hearing loss of the dorsal and ventral cochlear nucleus (DCN and VCN) and the inferior colliculus (IC) in adult mouse brain slices. Recordings showed a slight, but significant, elevation in spontaneous firing rates in DCN and VCN immediately after noise trauma, whereas no differences were found in IC. One week postexposure, neuronal responses remained unchanged compared to controls. At 14 days after noise trauma, intrinsic long-term hyperactivity in brain slices of the DCN and the IC was detected for the first time. Therefore, increase in spontaneous activity seems to develop within the period of two weeks, but not before day 7. The results give insight into the complex temporal neurophysiological alterations after noise trauma, leading to a better understanding of central mechanisms in noise-induced hearing loss.

Results of a multicenter clinical study evaluating a new Smart algorithm to measure neural response imaging.

OBJECTIVE: To evaluate the smart algorithm in speed and reliability of threshold estimation compared with the algorithm available in the standard fitting software and to evaluate the possibility of using programs based on the smart algorithm instead of programs derived from behavioral measures. PATIENTS: Twenty subjects unilaterally implanted with a CII Bionic Ear or HiRes90K device. INTERVENTIONS: Neural response imaging thresholds (tNRI) were measured using both the smart approach within the Research Studies Platform for Objective Measures and the SoundWave fitting software. Measurements were performed intraoperatively, at first fitting, and after 3 months of implant use. Each subject received a standard behavioral program and a SmartNRI program. Speech perception tests were conducted at 3 months, and subjective preferences were documented. MAIN OUTCOME MEASURES: Smart tNRI and SoundWave tNRI at each session; speech test results and subject preferences at the 3-month session. RESULTS: High correlations were found between smart tNRI and SoundWave tNRI. The time required to obtain NRI thresholds with the smart algorithm was a quarter of the time needed with SoundWave. Although most tested subjects preferred their behavioral programs, there were no significant differences in performance between SmartNRI and behavioral programs. CONCLUSION: Neural response imaging thresholds were obtained more rapidly with the smart algorithm than with SoundWave. Because no differences were observed between SmartNRI and behavioral programs, SmartNRI programs may be a useful alternative to behavioral programs in difficult to fit cases, where user feedback is sometimes difficult to obtain.

Sound-induced vertigo after cochlear implantation.

AIM: Postoperative vertigo is a well-known complication after cochlear implantation. The aim of the study was to investigate whether the electrical stimulation of the auditory structures via cochlear implant electrodes can affect the vestibular system and induce vertigo. MATERIALS AND METHODS: In the first group, 114 patients were surveyed retrospectively via questionnaires to evaluate the occurrence and frequency of sound-induced vertigo after cochlear implantation. In the second group of 26 patients, the effects of electrical stimulation on the vestibular system were studied prospectively. RESULTS: In the first group of patients without any preoperative sound-induced vertigo (n = 104), 20 patients (18%) reported sound-induced vertigo, which occurred after cochlear implantation. In the second group, an acoustic stimulus delivered via the speech processor of the cochlear implant elicited a vestibular evoked myogenic potential response in 4 of the 26 patients as a sign of vestibular costimulation (of the macula sacculi as part of the otolith organs). Horizontal and vertical nystagmus was triggered, whereas utricular function and postural stability remained unchanged. No correlation was found between C/M levels and the vestibular evoked myogenic potentials and nystagmus responses. CONCLUSION: Sound-induced vertigo can occur in cochlear implantees. This seems to be primarily caused by electrical costimulation of the sacculus as part of the otolith organs.

The possible impact of noise-induced Ca2+-dependent activity in the central auditory pathway: a manganese-enhanced MRI study.

Noise exposure at high intensities leads to a temporary shift of hearing thresholds (TTS) and is followed by a permanent threshold shift (PTS). Permanent threshold shift is not only associated with cochlear damage as the primary site-of-lesion, but also with subsequent structural and functional changes within the central auditory pathway. The aim of the present study was to monitor neuronal activity within central auditory structures in mice after noise exposure at different time intervals using manganese-enhanced magnetic resonance imaging (MEMRI). The results demonstrate for the first time that calcium-dependent activity patterns are modified in several structures of the central auditory system as the result of a noise-induced hearing loss (NIHL). The MEMRI data demonstrate that temporary threshold shift is correlated with an activity increase in hierarchically lower structures of the auditory pathway. This seems to be indicative of a direct noise impact at the first stage of central auditory processing. However, noise-dependent changes of higher auditory structures were found as well in the phase of PTS. Repeated noise exposure was found to induce an additional elevation of calcium-dependent activity in all investigated auditory structures - without a significant shift in auditory thresholds. Sustained manganese accumulation was present in the auditory brainstem after moderate acoustic stimulation as well without PTS induction. The long-lasting enhancement of MEMRI signals suggests a noise-induced activity increase of various calcium-dependent processes of different origin (such as neuroprotective mechanisms). The present findings could be helpful to better understand the time-course of different symptoms in NIHL and the individual susceptibility to noise.

Differential impact of temporary and permanent noise-induced hearing loss on neuronal cell density in the mouse central auditory pathway.

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.