Clinical Trial Details
— Status: Not yet recruiting
Administrative data
| NCT number |
NCT03713554 |
| Other study ID # |
HUM00137093 |
| Secondary ID |
|
| Status |
Not yet recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
November 15, 2024 |
| Est. completion date |
August 1, 2025 |
Study information
| Verified date |
June 2023 |
| Source |
University of Michigan |
| Contact |
Gregory Basura, M.D., Ph.D. |
| Phone |
734-936-8006 |
| Email |
gbasura[@]umich.edu |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
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.
Description:
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.
