Temporal Cortical Plasticity in Single-Sided Deafness: A Functional Imaging Study. Issue 8 (September 2015)

• Record Type: Journal Article
• Authors: Pross, Seth E.; Chang, Jolie L.; Mizuiri, Danielle; Findlay, Anne M.; Nagarajan, Srikantan S.; Cheung, Steven W.
• Is Part Of: Otology & neurotology. Volume 36:Issue 8(2015)
• Publication Date: 2015-09
• Subjects: Cortical plasticity -- Magnetoencephalography -- Single-sided deafness; Otology -- Periodicals; Ear -- Diseases -- Periodicals; Skull base -- Surgery -- Periodicals; 617.8005
• DOI: 10.1097/MAO.0000000000000821
• Languages: English
• ISSNs: 1531-7129

Abstract

Abstract : Hypothesis: To refine and extend the knowledge on cortical plasticity in single-sided deafness (SSD) by assessing magnetoencephalographic imaging in a well-defined group of subjects. Background: SSD causes difficulties with directional hearing, signal extraction in noise, and multispeaker identification and separation. In SSD, the ipsilateral auditory cortex is never powerfully driven by sound, which may lead to plastic change and contribute to higher-order psychoacoustic dysfunction beyond loss of a peripheral sound sensor. Study Design: A cross-sectional study on 12 subjects with long-term, adult-onset, nontraumatic SSD and 12 normal-hearing controls was conducted using magnetoencephalographic imaging, magnetic resonance imaging, and validated hearing instruments. Pure-tone stimuli at five frequencies were presented to each hearing ear individually. M100 activation peak times of the ipsilateral and contralateral auditory cortices were analyzed. Results: Controls showed an M100 interhemispheric mean latency difference of 6.6 milliseconds. In contrast, subjects with SSD exhibited a mean of 1.7 milliseconds. This loss of interhemispheric latency difference was statistically significant ( p < 0.05, analysis of variance with repeated measures). SSD subjects confirmed degraded hearing function on both Hearing Handicap Inventory for Adults ( p < 0.001) and Speech, Spatial, and Qualities of Hearing Scale instruments ( p < 0.001). Conclusion: SSD disrupts M100 latency difference between the two hemispheres to sound stimulation. This finding may represent maladaptive temporal cortical plasticity because of loss of a peripheral sensor. Based on this premise, a new generation of neurophysiologically inspired auditory treatments to correct or mitigate central consequences of SSD may be considered to optimize hearing in individuals with only one functional ear.