Human intracerebral potentials associated with target, novel, and omitted auditory stimuli

Abstract

We recorded late auditory potentials from lateral and medial regions in the frontal, temporal and parietal lobes of patients with temporal lobe epilepsy implanted with horizontal depth electrodes. Tone sequences were presented in three tasks: 1) auditory target detection in a tone sequence, 2) target detection with interspersed novel stimuli, and 3) detection of stimulus omissions. At frontal sites, potentials to targets showed a triphasic response with peak latencies around 200, 270 and 350 ms. At temporal sites, potentials consisted of a generally positive 285 ms peak which was sometimes accompanied by a negative peak at 200 ms or at 400 ms. At parietal sites, potentials were generally triphasic with latencies of about 230, 300, and 370 ms. At most sites, potentials evoked by novel stimuli had shorter latencies than those evoked by targets. The frontal and parietal potentials were either absent or strongly attenuated during stimulus omissions. The results lend further support to the multiple generator hypothesis of late potentials and suggest that some of the cerebral sources of the late potentials are stimulus dependent while others are not.

The Influence of Stimulus Deviance on Electrophysiologic and Behavioral Responses to Novel Events

“…In the patients with depth electrodes, the earliest response occurs in anterior regions (Baudena et al, 1995;Halgren et al, 1995a;Alain et al, 1989;. Consistent with this observation, the current study found that P3 latency in response to either simple or unusual deviant stimuli was shortest at frontal sites.…”

“…Lesion and depth electrode studies strongly indicate that the activity indexed by the surface novelty N2 -P3 is subserved by a distributed network that includes dorsolateral prefrontal cortex, anterior cingulate, temporal -parietal junction, and hippocampus (Baudena et al, 1995;Halgren et al, 1995a, Halgren et al, 1995bYamaguchi & Knight, 1991b;Alain et al, 1989;Knight, 1984Knight, , 1986Knight, , 1996Knight, , 1997Knight & Scabini, 1998). In the patients with depth electrodes, the earliest response occurs in anterior regions (Baudena et al, 1995;Halgren et al, 1995a;Alain et al, 1989;.…”

“…Interestingly, studies of stroke patients with focal lesions and seizure patients with depth electrodes suggest that the surface N2 -P3 evoked by novel stimuli results from the activity of a distributed neural network with critical components in frontal cortex (Daffner et al, 2000a, in press;Baudena et al, 1995;Halgren et al, 1995a, Halgren et al, 1995bYamaguchi & Knight, 1991b;Alain, Richer, Achim, & Saint Hilaire, 1989;Knight, 1984Knight, , 1986Knight, , 1996Knight, , 1997Knight & Scabini, 1998). In the patients with depth electrodes, the earliest response to deviant stimuli occurs in anterior regions (Baudena et al, 1995;Halgren et al, 1995a;Alain et al, 1989;. This observation led Halgren et al (Baudena et al, 1995;Halgren et al, 1995a) to argue that the N2 -P3a may reflect the activity of frontal networks comparing incoming stimuli with the current context held in working memory, and signaling deviation from it.…”

Differential Contribution of Frontal and Temporal Cortices to Auditory Change Detection: fMRI and ERP Results

“…This view is supported by recent findings demonstrating that patients with dorsolateral prefrontal lesions show a marked impairment in attentional control of irrelevant sensory input (Chao and Knight, 1997), as well as a reduction of the MMN, especially over the lesioned hemisphere (Alain et al, 1989;Alho et al, 1994). Moreover, studies using current source density mapping reported an additional generator of the MMN presumably located in the right frontal lobes (Giard et al, 1990, but see Deouell et al, 1998, for bilateral frontal contribution).…”

Frontal and Parietal Components of a Cerebral Network Mediating Voluntary Attention to Novel Events

“…Within this context, the P3 response to these novel stimuli (i.e., the novelty P3) has been interpreted as reflecting an involuntary, automatic process (Knight & Nakada, 1998;Knight & Scabini, 1998) involved in the orienting of attention to and/or the detection of deviant stimuli Hillyard, Picton, Plum, Mountcastle, & Geiger, 1987;Knight, 1984;Rohrbaugh, Parasuraman, & Davies, 1984;Naatanen, Gaillard, Gaillard, & Ritter, 1983;Snyder & Hillyard, 1976;Courchesne, Hillyard, & Galambos, 1975;Squires, Squires, & Hillyard, 1975;Roth, 1973;Ritter, Vaughan, & Costa, 1968). Using this type of novelty oddball paradigm, researchers have studied the cortical contributions to the surface novelty P3 response by investigating patients with focal lesions Knight, 1984Knight, , 1996Knight, , 1997Knight et al, 1989), patients undergoing evaluation with depth electrodes Halgren et al, 1995;Alain, Richer, Achim, & Saint Hilaire, 1989), and non-brain-damaged subjects using ERP source analysis (Spencer, Dien, & Donchin, 1999;Mecklinger & Ullsperger, 1995) or functional neuroimaging techniques (Clark, Fannon, Song, Randall, & Bauer, 2000;Hinton, MacFall, & McCarthy, 1999;Knight & Nakada, 1998;Ebmeier et al, 1995). These studies support the hypothesis that novelty processing involves a multifocal network with anatomical components in anterior and posterior regions.…”