Behavioral and event-related brain potential (ERP) measures were used to elucidate the neural mechanisms of involuntary engagement of attention by novelty and change in the acoustic environment. The behavioral measures consisted of the reaction time (RT) and performance accuracy (hit rate) in a forced-choice visual RT task where subjects were to discriminate between odd and even numbers. Each visual stimulus was preceded by an irrelevant auditory stimulus, which was randomly either a “standard” tone (80%), a slightly, higher “deviant” tone (10%), or a natural, “novel” sound (10%). Novel sounds prolonged the RT to successive visual stimuli by 17 msec as compared with the RT to visual stimuli that followed standard tones. Deviant tones, in turn, decreased the hit rate but did not significantly affect the RT. In the ERPs to deviant tones, the mismatch negativity (MMN), peaking at 150 msec, and a second negativity, peaking at 400 msec, could be observed. Novel sounds elicited an enhanced N1, with a probable overlap by the MMN, and a large positive P3a response with two different subcomponents: an early centrally dominant P3a, peaking at 230 msec, and a late P3a, peaking at 315 msec with a right-frontal scalp maximum. The present results suggest the involvement of two different neural mechanisms in triggering involuntary attention to acoustic novelty and change: a transient-detector mechanism activated by novel sounds and reflected in the N1 and a stimulus-change detector mechanism activated by deviant tones and novel sounds and reflected in the MMN. The observed differential distracting effects by slightly deviant tones and widely deviant novel sounds support the notion of two separate mechanisms of involuntary attention.

This article reviews recent event-related brain potential (ERP) studies of involuntary attention and distractibility in response to novelty and change in the acoustic environment. These studies show that the mismatch negativity, N1 and P3a ERP components elicited by deviant or novel sounds in an unattended sequence of repetitive stimuli index different processes along the course to involuntary attention switch to distracting stimuli. These studies used new auditory-auditory and auditory-visual distraction paradigms, which enable one to assess objectively abnormal distractibility in several clinical patient groups, such as those suffering from closed-head injuries or chronic alcoholism.

Infrequent (“deviant”) sounds occurring in a sequence of repetitive (“standard”) sounds elicit an event-related brain potential (ERP) response called the mismatch negativity (MMN) even in the absence of attention to these sounds. MMN appears to be caused by a neuronal mismatch between the deviant auditory input and a sensory-memory trace representing the standard stimuli. This automatic mismatch process has presumably a central role in discrimination of changes in the acoustic environment outside the focus of attention. Thus, localizing cerebral generators of MMN might help identify brain mechanisms of auditory sensory memory and involuntary attention. This review summarizes results from studies aimed at localizing MMN generators on the basis of (1) scalp-distribution, (2) magnetoencephalographic (MEG), (3) intracranial, and (4) brain-lesion data. These studies indicate that a major MMN source is located in the auditory cortex. However, the exact location of this MMN generator appears to depend on which feature of a sound is changed (e.g., frequency, intensity, or duration), as well as on the complexity of the sound (e.g., a simple tone versus complex sound). Consequently, memory traces for different acoustic features, as well as for sounds of different complexity, might be located in different regions of auditory cortex. However, MMN appears to have generators in other brain structures, too. There is some evidence for contribution of frontal-lobe activity to the MMN, which might be related to the involuntary switching of attention to a stimulus change occurring outside the focus of attention. In addition, intracranial MMN recordings in animals suggest that at least in some species, MMN subcomponents also may be generated in the thalamus and hippocampus.