<p>Sensory loss is prevalent in older adults and is associated with changes to brain structure and function. In early life, the brain compensates for sensory loss by upregulating intact senses, such as in deafness where neural sensitivity for vision increases and visual peripheral perception improves. However, it is unclear if similar neuroplastic compensation occurs in older adults with sensory loss, which would show the aging brain’s adaptability and inform sensory rehabilitation strategies. We tested for evidence of compensatory visual neuroplasticity in adults (<i>N</i> = 66) aged 53 to 80 with typical hearing or hearing loss, and if this neuroplasticity differed for visual stimuli that were or were not relevant to speech perception. Participants viewed speech-like or non-speech stimuli as we recorded cortical activity with the 64-channel electroencephalogram (EEG). Participants with more hearing loss tended to have longer cortical P1 and N1 latencies in the visual evoked potential. However, the later cortical P2 response latency decreased with more hearing loss in agreement with compensatory plasticity. Effects were independent of numerical age. Latency effects in hearing loss were more pronounced for the speech-like stimulus compared to the non-speech stimulus, but P2 responses for the non-speech stimulus showed greater cross-modal recruitment of the temporal cortex. Findings show for the first time that compensatory plasticity operates on later cortical P2 responses in older adults, is not explained by numerical age, and differs for speech and non-speech events. However, P1 and N1 responses in networks coding for visual speech may be sensitive to sensory decline.</p>

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Visual cortical responses in age-related hearing loss show evidence for compensatory neuroplasticity

  • Patricia V. Aguiar,
  • Michelle R. Williams,
  • Brandon T. Paul

摘要

Sensory loss is prevalent in older adults and is associated with changes to brain structure and function. In early life, the brain compensates for sensory loss by upregulating intact senses, such as in deafness where neural sensitivity for vision increases and visual peripheral perception improves. However, it is unclear if similar neuroplastic compensation occurs in older adults with sensory loss, which would show the aging brain’s adaptability and inform sensory rehabilitation strategies. We tested for evidence of compensatory visual neuroplasticity in adults (N = 66) aged 53 to 80 with typical hearing or hearing loss, and if this neuroplasticity differed for visual stimuli that were or were not relevant to speech perception. Participants viewed speech-like or non-speech stimuli as we recorded cortical activity with the 64-channel electroencephalogram (EEG). Participants with more hearing loss tended to have longer cortical P1 and N1 latencies in the visual evoked potential. However, the later cortical P2 response latency decreased with more hearing loss in agreement with compensatory plasticity. Effects were independent of numerical age. Latency effects in hearing loss were more pronounced for the speech-like stimulus compared to the non-speech stimulus, but P2 responses for the non-speech stimulus showed greater cross-modal recruitment of the temporal cortex. Findings show for the first time that compensatory plasticity operates on later cortical P2 responses in older adults, is not explained by numerical age, and differs for speech and non-speech events. However, P1 and N1 responses in networks coding for visual speech may be sensitive to sensory decline.