Congenital amusia is a lifelong disorder characterized by a difficulty in perceiving and producing music despite normal intelligence and hearing. Behavioral data have indicated that it originates from a deficit in fine-grained pitch discrimination, and is expressed by the absence of a P3b event-related brain response for pitch differences smaller than a semitone and a bigger N2b-P3b brain response for large pitch differences as compared to controls. However, it is still unclear why the amusic brain overreacts to large pitch changes. Furthermore, another electrophysiological study indicates that the amusic brain can respond to changes in melodies as small as a quarter-tone, without awareness, by exhibiting a normal mismatch negativity (MMN) brain response. Here, we re-examine the event-related N2b-P3b components with the aim to clarify the cause of the larger amplitude observed by Peretz, Brattico, and Tervaniemi (2005), by experimentally matching the number of deviants presented to the controls according to the number of deviants detected by amusics. We also re-examine the MMN component as well as the N1 in an acoustical context to investigate further the pitch discrimination deficit underlying congenital amusia. In two separate conditions, namely ignore and attend, we measured the MMN, the N1, the N2b and the P3b to tones that deviated by an eight of a tone (25 cents) or whole tone (200 cents) from a repeated standard tone. The results show a normal MMN, a seemingly normal N1, a normal P3b for the 200 cents pitch deviance, and no P3b for the small 25 cents pitch differences in amusics. These results indicate that the amusic brain responds to small pitch differences at a pre-attentive level of perception, but is unable to detect consciously those same pitch deviances at a later attentive level. The results are consistent with previous MRI and fMRI studies indicating that the auditory cortex of amusic individuals is functioning normally. (Contains 2 tables and 4 figures.)