Date of Degree


Document Type


Degree Name





Gerard Bruder

Committee Members

Craig Tenke

Jürgen Kayser

Joshua Brumberg

Subject Categories



Mismatch negativity (MMN) studies provide insights into the brain's ability to perceive and/or detect deviations from established sensory patterns. Clinical studies investigating the loudness-dependency of auditory evoked potential (LDAEP) have shown a relationship between the intensity of an auditory stimulus and neuro-physiological or -chemical activity of the primary auditory cortex. Unfortunately, these two bodies of literature remain disjointed. The present study integrates elements of each body of literature to a) investigate the impact of varying levels of intensity deviance on N1/P2 with a standard set of intensities used in LDAEP paradigms, and b) assess the extent to which deviance-related processes (indexed by MMN) are affected by louder or softer tones. A passive MMN-paradigm used the same stimuli as deviants and standards in order to separate deviance- from stimulus-specific N1/P2 processes. A CSD-PCA approach was used to identify and quantify reference-independent patterns of activity underlying the ERP. Results show that the intensity dependence of N1/P2 is largely dependent on the context in which a given intensity was cast. Namely, a high rate of repetitions of standard intensities produce significant reductions (adaptations) in N1/P2, while N1/P2 enhancement occurred for louder, but not softer deviants. Moreover, MMN amplitude paralleled intensity disparity; however, louder deviants produced greater MMN activity than softer deviants, Intensity Modulation of N1 and MMN presumably reflecting an attentional modulation of sensory processing. A P3a-like vertex source was elicited by the loudest intensity (100 dB), but was absent for all other intensities. Insights gained from this study have direct implications for both clinical LDAEP and MMN studies. LDAEP studies should consider how overlapping or dynamic processes (e.g., adaptation of N1/P2 or elicitation of MMN) influence the amplitudes of N1 and P2. MMN studies should a) consider how attention may interact with intensity to produce distinctly different MMN responses independent of actual deviance-related processes, b) consider how P3a activity reflects a wider range of functions other than 'attentional signaling,' such as response inhibition or startle-related processes, and c) consider other physiologically plausible and parsimonious explanations of MMN (e.g., sensory adaptation) when interpreting findings.


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