The effect of increased listening effort on the balance performance of patients with compensated vestibular lesion.

OBJECTIVES: This study investigated the effects of listening effort (LE) on balance in patients with compensated vestibular deficits compared to healthy peers. METHODS: The subjects included two main groups: a control group of 15 healthy subjects and a study group of 19 patients with compensated vestibular pathology. The computerized dynamic posturography test (CDP) was conducted without the speech-in-noise task as a baseline, then the participant was subjected to a dual task in which the auditory task (speech-in-noise sentences) was given as the primary task, and the balance function test was the secondary task. RESULTS: WITHIN-GROUP ANALYSIS: The study group showed statistically significantly worse values of all body balance parameters under dual-task than the baseline in all conditions. These differences were much higher under the compliant platform conditions. However, these findings were not statistically significant in the control group. BETWEEN-GROUP ANALYSIS: The study group showed a statistically significant decline in body balance reactions compared to the control group under dual-task with increased listening effort and the compliant platform. Study subgroup analysis revealed statistically significant differences between patients with unilateral vestibular loss (UVL) and those with bilateral vestibular loss (BVL) in the unstable platform condition. CONCLUSION: Our study regarding implementing a dual-tasking paradigm as a measure of LE during the evaluation of chronic vestibular patients with CDP demonstrated how dual-tasking with increased LE affects postural stability. Because of this, patients will probably be more prone to tripping and falling in multitasking situations, as found in real-world settings. This fact should be taken into consideration while testing patients with chronic vertigo and compensated states at VNG. A dual-task paradigm helps uncover the unrevealed pathology.

Transplantation of adipose-derived stromal cells protects functional and morphological auditory nerve integrity in a model of cochlear implantation.

Cochlear implants are considered the gold standard therapy for subjects with severe hearing loss and deafness. Cochlear implants bypass the damaged hair cells and directly stimulate spiral ganglion neurons (SGNs) of the auditory nerve. Hence, the presence of functional SGNs is crucial for speech perception in electric hearing with a cochlear implant. In deaf individuals, SGNs progressively degenerate due to the lack of neurotrophic support, normally provided by sensory cells of the inner ear. Adipose-derived stromal cells (ASCs) are known to produce neurotrophic factors. In a guinea pig model of sensory hearing loss and cochlear implantation, ASCs were autologously transplanted into the scala tympani prior to insertion of a cochlear implant on one side. Electrically evoked auditory brain stem responses (eABR) were recorded 8 weeks after cochlear implantation. At conclusion of the experiment, the cochleae were histologically evaluated. Compared to untreated control animals, transplantation of ASCs resulted in an increased number of SGNs and their peripheral neurites. In ASC-transplanted animals, mean eABR thresholds were lower and suprathreshold amplitudes larger, suggesting a larger population of intact auditory nerve fibers. Moreover, when compared to controls, amplitude-level functions of eABRs in ASC transplanted animals demonstrated steeper slopes in response to increasing interphase gaps (IPGs), indicative of better functionality of the auditory nerve. In summary, results suggest that transplantation of autologous ASCs into the deaf inner ear may have protective effects on the survival of SGNs and their peripheral processes and may thus contribute to long-term benefits in speech discrimination performance in cochlear implant subjects.

Adipose-derived stromal cells enhance auditory neuron survival in an animal model of sensory hearing loss.

BACKGROUND: A cochlear implant (CI) is an electronic prosthesis that can partially restore speech perception capabilities. Optimum information transfer from the cochlea to the central auditory system requires a proper functioning auditory nerve (AN) that is electrically stimulated by the device. In deafness, the lack of neurotrophic support, normally provided by the sensory cells of the inner ear, however, leads to gradual degeneration of auditory neurons with undesirable consequences for CI performance. METHODS: We evaluated the potential of adipose-derived stromal cells (ASCs) that are known to produce neurotrophic factors to prevent neural degeneration in sensory hearing loss. For this, co-cultures of ASCs with auditory neurons have been studied, and autologous ASC transplantation has been performed in a guinea pig model of gentamicin-induced sensory hearing loss. RESULTS: In vitro ASCs were neuroprotective and considerably increased the neuritogenesis of auditory neurons. In vivo transplantation of ASCs into the scala tympani resulted in an enhanced survival of auditory neurons. Specifically, peripheral AN processes that are assumed to be the optimal activation site for CI stimulation and that are particularly vulnerable to hair cell loss showed a significantly higher survival rate in ASC-treated ears. DISCUSSION/CONCLUSION: ASC transplantation into the inner ear may restore neurotrophic support in sensory hearing loss and may help to improve CI performance by enhanced AN survival.