Biomedical subjects

Guido P H Band

Publications and source records attributed to Guido P H Band.

5 recordsLinked to original sources

PubMed2004

ERP components associated with successful and unsuccessful stopping in a stop-signal task.

The primary aim of this study was to examine how response inhibition is reflected in components of the event-related potential (ERP), using the stop-signal paradigm as a tool to manipulate response inhibition processes. Stop signals elicited a sequence of N2/P3 components that partly overlapped with ERP components elicited by the reaction stimulus. N2/P3 components were more pronounced on stop-signal trials than on no-stop-signal trials. At Cz, the stop-signal P3 peaked earlier on successful than on unsuccessful stop trials. This finding extends the horse race model by demonstrating that the internal response to the stop signal (as reflected in stop-signal P3) is not constant, but terminates at different moments in time on successful and unsuccessful stop trials. In addition, topographical distributions and dipole analysis of high density EEG recordings indicated that different cortical generators were involved in P3s elicited on successful and unsuccessful stop-signal trials. The latter results suggest that P3 on successful stop-signal trials not only reflects stop-signal processing per se, but also efficiency of inhibitory control.

Adolescent↗

PubMed2003

Speed-accuracy modulation in case of conflict: the roles of activation and inhibition.

This study investigated how the speed-accuracy balance is modulated by changes in the time course of motor activation and inhibition of a primed response. Responses and event-related brain potentials were recorded in a paradigm in which the first stimulus indicated the correct response with 80% validity. The remaining 20% of the trials required no response (no-go) or a response opposite to the cued hand (change trials). Subjects were instructed either to balance speed and accuracy or to emphasize speed at the cost of accuracy. Analyses of error patterns, reaction time distributions and brain potentials show that subjects can modulate the amount of activation of the primed response. More surprisingly, the engagement of inhibition of the response also varied with the speed-accuracy instruction. The results are consistent with a model where the frontothalamic loop actively controls both the activation and the inhibition of responses, depending on the current task requirements.

Adult↗

PubMed2003

Horse-race model simulations of the stop-signal procedure.

In the stop-signal paradigm, subjects perform a standard two-choice reaction task in which, occasionally and unpredictably, a stop-signal is presented requiring the inhibition of the response to the choice signal. The stop-signal paradigm has been successfully applied to assess the ability to inhibit under a wide range of experimental conditions and in various populations. The current study presents a set of evidence-based guidelines for using the stop-signal paradigm. The evidence was derived from a series of simulations aimed at (a) examining the effects of experimental design features on inhibition indices, and (b) testing the assumptions of the horse-race model that underlies the stop-signal paradigm. The simulations indicate that, under most conditions, the latency, but not variability, of response inhibition can be reliably estimated.

Animals↗

PubMed2002

Alcohol consumption impairs detection of performance errors in mediofrontal cortex.

The anterior cingulate cortex (ACC) is a critical component of the human mediofrontal neural circuit that monitors ongoing processing in the cognitive system for signs of erroneous outcomes. Here, we show that the consumption of alcohol in moderate doses induces a significant deterioration of the ability to detect the activation of erroneous responses as reflected in the amplitude of brain electrical activity associated with the ACC. This impairment was accompanied by failures to instigate performance adjustments after these errors. These findings offer insights into how the effects of alcohol on mediofrontal brain function may result in compromised performance.

Adult↗

PubMed2002

Explaining neurocognitive aging: is one factor enough?

As an introduction to the special issue on neurocognitive factors underlying age effects, we discuss a number of recent developments in the literature on aging. The classic distinction between generalized and process-specific cognitive changes with old age has reappeared in the distinctions between the frontal lobe hypothesis and more differentiated views of neurocognitive aging. We argue that neurological decay in the frontal cortex has important implications for cognitive control, but that the frontal lobe hypothesis does not capture the plethora of changes that characterize aging and incorrectly suggests a unitary effect.

Aged↗