The NoGo P300 ‘anteriorization’ effect and response inhibition

Salisbury, Dean F.; Griggs, Carlye B.; Shenton, Martha E.; McCarley, Robert W.

doi:10.1016/j.clinph.2004.01.028

Cited by 94 publications

(70 citation statements)

References 31 publications

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“…Furthermore, our paradigm as well as Van der Stelt's only allows us to examine the P3b wave (a response elicited by the target stimuli that require a response from the subject). More complex P300 experiments incorporating additional infrequent novel stimuli that generate the P3a response would be worth investigating in the prodrome (Araki et al, 2006;Frodl-Bauch et al, 1999;Laurens et al, 2005;Mathalon et al, 2000;Salisbury et al, 2004;Salisbury et al, 2001;Sponheim et al, 2006;Sumich et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…The P300 wave reflects cortical activity during a form of continuous performance task in which subjects respond to target stimuli embedded at random in a sequence of standard stimuli. This event-related potential is more specifically known as the P3b in order to distinguish it from the P3a, a response to task-irrelevant novel infrequent stimuli not examined in this paper (Araki et al, 2006;Frodl-Bauch et al, 1999;Laurens et al, 2005;Mathalon et al, 2000;Salisbury et al, 2004;Salisbury et al, 2001;Sponheim et al, 2006). Another EEG marker investigated here, the N100 wave, reflects the early phase of attentive stimulus processing (Boutros et al, 2004;McCarley et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Abnormal P300 in people with high risk of developing psychosis

et al. 2008

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Background: Individuals with an "At Risk Mental State" (or "prodromal" symptoms) have a 20-40% chance of developing psychosis; however it is difficult to predict which of them will become ill on the basis of their clinical symptoms alone. We examined whether neurophysiological markers could help to identify those who are particularly vulnerable.Method: 35 cases meeting PACE criteria for the At Risk Mental State (ARMS) and 57 controls performed an auditory oddball task whilst their electroencephalogram was recorded. The latency and amplitude of the P300 and N100 waves were compared between groups using linear regression.Results: The P300 amplitude was significantly reduced in the ARMS group [8.6 ±6.4 microvolt] compared to controls [12.7 ±5.8 microvolt] (p<0.01). There were no group differences in P300 latency or in the amplitude and latency of the N100. Of the at-risk subjects that were followed up, seven (21%) developed psychosis. Please find attached a fully revised manuscript titled "Abnormal P300 in people with high risk of developing psychosis". We also enclose a letter with the comments from the reviewers and our detailed answers on how we have done all the changes requested. (t-test; p=0.93). Those making a transition to psychosis were marginally more educated but this was only at trend level with a 3 year average difference in the age at which they completed their studies (t-test; p=0.07).Similarly, logistic regression analyses showed that compared to those who remained at risk, the seven cases who made a transition to psychosis had no significant differences in P300 amplitude/latency or N100 amplitude/latency (p values ranging from 0.30 to 0.63 for all four analyses). We have reported these comparisons very concisely and cautiously because referee #2 said that these analyses with only 7 individual making a transition were preliminary and power is limited. Please see results section paragraph 2. RESPONSE TO REVIEWER #2:Thank you for your suggestions, which have improved the paper. Below are your comments in blue-italics and how we have amended the manuscript accordingly in black with cross-references to the revised manuscript.This paper addresses an important and timely topic, namely, whether auditory P300 is reduced in subjects with at risk mental states and whether the P300 predicts subsequent conversion to psychosis. The study finds a significant deficit in P300 in ARMS subjects, relative to controls, replicating a previously a previously published report. The study had the potential to incrementally * 2. Response to Reviews 2 contribute to the literature by examining the utility of baseline P300 deficits as a predictor of subsequent conversion to psychosis; however, the negative finding coupled with the lack of power for this analysis (only 7 converters) make this aspect of the study inconclusive. More detailed comments are provided below:We have added a paragraph in the discussion to acknowledge the limitation of our small group of converters and how we have low statistical power to compa...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Abnormal P300 in people with high risk of developing psychosis

et al. 2008

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“…The topographic distribution for this component is somewhat more central than the parietal P300 from the target stimulus. The no-go P300 has been linked to response inhibition mechanisms, although this hypothesis is debated (Azizian et al, 2006;Eimer, 1993;Falkenstein et al, 2000;Salisbury et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Updating P300: An integrative theory of P3a and P3b

Polich

2007

Clinical Neurophysiology

6,465

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The empirical and theoretical development of the P300 event-related brain potential (ERP) is reviewed by considering factors that contribute to its amplitude, latency, and general characteristics. The neuropsychological origins of the P3a and P3b subcomponents are detailed, and how target/ standard discrimination difficulty modulates scalp topography is discussed. The neural loci of P3a and P3b generation are outlined, and a cognitive model is proffered: P3a originates from stimulusdriven frontal attention mechanisms during task processing, whereas P3b originates from temporalparietal activity associated with attention and appears related to subsequent memory processing. Neurotransmitter actions associating P3a to frontal/dopaminergic and P3b to parietal/norepinephrine pathways are highlighted. Neuroinhibition is suggested as an overarching theoretical mechanism for P300, which is elicited when stimulus detection engages memory operations.

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“…Based on these findings, the NGA may be considered as a noninvasive electrophysiological measurement of medial prefrontal brain function involved in response inhibition processes. This association with response inhibition, however, is still under debate and may even be absent in the auditory modality (Salisbury et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

DTNBP1 (Dysbindin) Gene Variants Modulate Prefrontal Brain Function in Healthy Individuals

Fallgatter

Herrmann

Hohoff

et al. 2006

Neuropsychopharmacol

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DTNBP1 (dysbindin) is one of the several putative schizophrenia genes supported by association, neuroanatomical, and cellular studies. These suggest an involvement of DTNBP1 in the prefrontal cortex and cognitive functions mediated by interaction with neurotransmitter systems, in particular glutamate. The influence of DTNBP1 gene variation on prefrontal brain function at the systemic neurophysiological level, though, has not been characterized. The NoGo-anteriorization (NGA) as an event-related potential (ERP) measure elicited during the continuous performance test (CPT) has been established as a valid neurophysiological parameter for prefrontal brain function in healthy individuals and patients with schizophrenias. In the present study, we therefore investigated the influence of eight dysbindin gene variants on the NGA as a marker of prefrontal brain function in 48 healthy individuals. Two DTNBP1 polymorphisms previously linked to schizophrenia (P1765 and P1320) were found associated with changes in the NGA. Post hoc analysis showing an influence of genetic variation at these loci on the Go centroid and frontal amplitudes suggest that this might be due to modification of the execution of motor processes by the prefrontal cortex. This is the first report on a role of DTNBP1 gene variation for prefrontal brain function at a systemic neurophysiological level in healthy humans. Future studies will have to address the relevance of this observation for patients with schizophrenias.

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The NoGo P300 ‘anteriorization’ effect and response inhibition

Cited by 94 publications

References 31 publications

Abnormal P300 in people with high risk of developing psychosis

Abnormal P300 in people with high risk of developing psychosis

Updating P300: An integrative theory of P3a and P3b

DTNBP1 (Dysbindin) Gene Variants Modulate Prefrontal Brain Function in Healthy Individuals

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