Sudden onset, profound unilateral sensorineural hearing loss, or single-sided deafness (SSD) is common (60,000 annually in US). Permanent SSD leads to listener disability and long-term challenges with sound localization and speech perception. The only definitive auditory rehabilitation for SSD is a cochlear implant (CI). Limited research on optimal timing for CI after SSD exists since insurance authorization typically requires bilateral deafness for CI placement. Secondly, limited CI compatible brain imaging technology exists to investigate changes pre- and post-CI in SSD. Thus, lack of systematic research results in random CI placement in SSD with inconsistent auditory performance that may be due, in part, to variable neural activation in primary auditory cortex (A1). Animal models and humans with SSD show enhanced A1 neural responses with sound stimulation of the remaining only-hearing ear1,2. Also, cross-modal plasticity3 (increased A1 neural responses to non-auditory sensory systems) leads to preferential A1 activation to somatosensory and visual stimuli4,5,6 in SSD. Essentially, non-auditory sensory systems recruit A1 neurons away to become responsive to new non-auditory stimulation. This limits the ability of A1 neurons to respond to auditory stimulation once CI rehabilitation is implemented. Importantly, a sensitive time window after SSD when these brain changes occur may impact A1 neural auditory responses and ultimately CI performance and speech perception.~Activation strength of A1 neurons is associated with optimal CI speech recognition and performance7,8. The investigators predict that if A1 neurons opposite SSD are kept active by increased sensitivity to only-hearing ear stimulation after SSD they would be less likely to be reassigned to non-auditory cross-modal plasticity. Alternatively, if only-hearing ear inputs to A1 are not sufficient, or if more somatosensory and/or visual inputs occur after SSD, fewer A1 neurons will be available to respond to CI stimulation and speech performance may suffer. The objective of these studies is first, to understand the timing and nature of both A1 cross-modal plasticity (sensitivity to somatosensory and/or visual systems) and only-hearing ear pathway enhancement in SSD. Second, is to examine the impact of CI on reversing these changes that may affect CI performance.~Human research on SSD and CI is sparse due to inadequate brain imaging technology that can measure A1 neural activity that is also CI compatible. Functional near-infrared spectroscopy (fNIRS) and event-related potentials (ERPs) with electroencephalography (EEG), when used together, can capture localization (fNIRS) and timing (EEG) of correlates of A1 neural responses (fNIRS) to distinguish between the effects of cross-modal and only-hearing ear stimulation pre- and post-CI. Using stimulation/silence block recording conditions in SSD adults, A1 hemodynamic responses (correlates of neural activity) and resting state functional cortical connectivity (RSFC; index of inter-cortical connections) will be measured with fNIRS and ERPs and correlated with only-hearing ear and cross-modal plasticity9,10 and CI speech performance11.~Specific Aim 1: Determine when A1 neural plasticity occurs following SSD onset. The timing of brain changes that may influence hearing rehabilitation within human A1 after SSD is not known. The goal of this aim is to identify plasticity that occurs when there is no CI intervention and characterize when A1 neurons are either influenced by only-hearing ear, somatosensory and/or visual inputs after SSD. Experiment 1. A1 hemodynamic responses (fNIRS correlate of neural activity) and changes in brain RSFC and ERPs to somatosensory, visual and only-hearing ear stimulation will be recorded 1, 3, 6, 9 and 12 months after SSD onset. The investigators predict cross-modal plasticity and A1 responses to only-hearing ear stimulation after SSD will have specific timing patterns of onset.~Specific Aim 2: Identify changes in A1 neural plasticity that follows CI rehabilitation.~The goal of this aim is to determine how and when CI placement affects A1 plasticity in SSD. As such, the investigators will determine when and if brain changes can be prevented that may hinder eventual CI performance. Experiment 2: Participants following CI placement that is either early- (<6mos), delayed- (6-12mos) or late- (>12mos-5yrs) after SSD and random insurance authorization will be analyzed for hemodynamic responses, changes in RSFC and ERPs to somatosensory, visual, CI, and only-hearing ear stimulation 1-12 months after CI. The investigators predict optimal CI speech performance will be associated with stronger fNIRS/ERP responses to early- and mid-CI placement that will reverse A1 responses to cross-modal stimulation.~Specific Aim 3: Identify neurocognitive profiles of successful CI rehabilitation of SSD. A1 plasticity pre- and post-CI and its relationship to speech performance in SSD will be measured. Experiment 3: CI speech performance testing will be conducted and results are expected to correlate with degrees/timing of plasticity from Aims 1 and 2. The investigators predict those with less A1 cross-modal plasticity and greater responses to the only-hearing ear will show better CI speech performance, while greater A1 responses to somatosensory and/or visual stimulation will perform more poorly with CI.~Clinical Significance: The investigators predict that this project will uncover timing and mechanisms of key auditory brain plasticity that follows adult-onset SSD and CI rehabilitation. This work will also demonstrate that fNIRS may prove to be a superior measure of A1 plasticity that could be used going forward to improve the timing of placement of CI for SSD to optimize speech performance and auditory rehabilitation.
The timing of brain changes that may influence hearing rehabilitation within human A1 after single-sided deafness (SSD) is not known. The goal is to determine when A1 neural plasticity occurs following SSD onset.