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Neural Plasticity
Volume 2014, Article ID 127824, 16 pages
http://dx.doi.org/10.1155/2014/127824
Research Article

Modulation of Electrocortical Brain Activity by Attention in Individuals with and without Tinnitus

1Department of Psychology, Neuroscience & Behaviour, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1
2Department of Electrical and Computer Engineering, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1
3McMaster Institute for Music and the Mind, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1

Received 27 March 2014; Accepted 15 April 2014; Published 12 June 2014

Academic Editor: Aage Møller

Copyright © 2014 Brandon T. Paul et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Age and hearing-level matched tinnitus and control groups were presented with a 40 Hz AM sound using a carrier frequency of either 5 kHz (in the tinnitus frequency region of the tinnitus subjects) or 500 Hz (below this region). On attended blocks subjects pressed a button after each sound indicating whether a single 40 Hz AM pulse of variable increased amplitude (target, probability 0.67) had or had not occurred. On passive blocks subjects rested and ignored the sounds. The amplitude of the 40 Hz auditory steady-state response (ASSR) localizing to primary auditory cortex (A1) increased with attention in control groups probed at 500 Hz and 5 kHz and in the tinnitus group probed at 500 Hz, but not in the tinnitus group probed at 5 kHz (128 channel EEG). N1 amplitude (this response localizing to nonprimary cortex, A2) increased with attention at both sound frequencies in controls but at neither frequency in tinnitus. We suggest that tinnitus-related neural activity occurring in the 5 kHz but not the 500 Hz region of tonotopic A1 disrupted attentional modulation of the 5 kHz ASSR in tinnitus subjects, while tinnitus-related activity in A1 distributing nontonotopically in A2 impaired modulation of N1 at both sound frequencies.