Research Article Modulation of Electrocortical Brain Activity by Attention in Individuals with and without Tinnitus Brandon T. Paul, 1 Ian C. Bruce, 1,2,3 Daniel J. Bosnyak, 1,3 David C. Thompson, 1 and Larry E. Roberts 1,3 1 Department of Psychology, Neuroscience & Behaviour, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1 2 Department of Electrical and Computer Engineering, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1 3 McMaster Institute for Music and the Mind, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1 Correspondence should be addressed to Larry E. Roberts; roberts@mcmaster.ca Received 27 March 2014; Accepted 15 April 2014; Published 12 June 2014 Academic Editor: Aage Møller Copyright © 2014 Brandon T. Paul et al. his 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. Age and hearing-level matched tinnitus and control groups were presented with a 40Hz 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 ater 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. he 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 5kHz ASSR in tinnitus subjects, while tinnitus-related activity in A1 distributing nontonotopically in A2 impaired modulation of N1 at both sound frequencies. 1. Introduction Forms of neural plasticity are expressed by many neurons in central auditory structures and are believed to sculpt the neural changes that underlie the development of tinnitus and hyperacusis associated with hearing loss [1, 2]. Examples of neural changes attributed to neural plasticity in animal models include upregulation of somatosensory inputs to principal neurons in the dorsal cochlear nucleus (DCN) following section of the cochlear nerve [3] and broadening of the temporal integration window of spike-timing dependent plasticity for neurons in the DCN [4] and auditory cortex [5] in animals exhibiting behavioral evidence of tinnitus. Neural changes taking place ater deaferentation may in turn afect how neural activity is modiied when auditory training is applied to individuals with tinnitus, as is done by sound therapies intended to treat this condition. Roberts et al. [6] trained individuals with tinnitus and age and hearing- level matched controls to detect an auditory target embedded in a 5 kHz 40 Hz amplitude modulated (AM) sound. he 5 kHz 40 Hz AM sound was in the tinnitus frequency region (TFR) of the tinnitus subjects and evoked the stimulus-driven 40 Hz auditory steady response (ASSR) known to localize to sources in primary auditory cortex (A1) [7–10]. In agreement with earlier results obtained from normal hearing subjects [11, 12], the phase of the ASSR phase (the time delay between the 40 Hz stimulus and response waveforms) decreased progressively over training sessions in the control group, but ASSR phase did not change in the tinnitus group. In contrast, the amplitude of the ASSR (which was known from earlier research to be resistant to change) did not increase with training in controls, but ASSR amplitude increased with training in the tinnitus group, as did online ratings of the loudness of their tinnitus percept. It was suggested that abnormal synchronous neural activity underlying the tinnitus percept may have obstructed changes in ASSR phase in the tinnitus group, whereas reduced inhibition in A1 associated with tinnitus may have permitted an expansion of Hindawi Publishing Corporation Neural Plasticity Volume 2014, Article ID 127824, 16 pages http://dx.doi.org/10.1155/2014/127824