The P300 as a Marker of Waning Attention and Error Propensity

Action errors can occur when routine responses are triggered inappropriately by familiar cues. Here, EEG was recorded as volunteers performed a “go/no-go” task of long duration that occasionally and unexpectedly required them to withhold a frequent, routine response. EEG components locked to the onset of relevant go trials were sorted according to whether participants erroneously responded to immediately subsequent no-go trials or correctly withheld their responses. Errors were associated with a significant relative reduction in the amplitude of the preceding P300, that is, a judgement could be made bout whether a response-inhibition error was likely before it had actually occurred. Furthermore, fluctuations in P300 amplitude across the task formed a reliable associate of individual error propensity, supporting its use as a marker of sustained control over action

The p300 as a marker of waning attention and error propensity.

Action errors can occur when routine responses are triggered inappropriately by familiar cues. Here, EEG was recorded as volunteers performed a "go/no-go" task of long duration that occasionally and unexpectedly required them to withhold a frequent, routine response. EEG components locked to the onset of relevant go trials were sorted according to whether participants erroneously responded to immediately subsequent no-go trials or correctly withheld their responses. Errors were associated with a significant relative reduction in the amplitude of the preceding P300, that is, a judgement could be made bout whether a response-inhibition error was likely before it had actually occurred. Furthermore, fluctuations in P300 amplitude across the task formed a reliable associate of individual error propensity, supporting its use as a marker of sustained control over action.Peer Reviewe

Deficient sustained attention to response task and P300 characteristics in early Huntington’s disease

Evidence for the extent and nature of attentional impairment in premanifest and manifest Huntington’s disease (HD) is inconsistent. Understanding such impairments may help to better understand early functional changes in HD and could have consequences concerning care for HD patients. We investigated attentional control in both early and premanifest HD. We studied 17 early HD subjects (mean age: 51 years), 12 premanifest HD subjects (mean age: 43 years), and 15 healthy controls (mean age: 51 years), using the sustained attention to response task (SART), a simple Go/No-go test reflecting attentional and inhibitory processes through reaction time (RT) and error rates. Simultaneously recorded EEG yielded P300 amplitudes and latencies. The early HD group made more Go errors (p < 0.001) and reacted slower (p < 0.005) than the other groups. The RT pattern during the SART was remarkably different for early HD subjects compared to the other two groups (p < 0.005), apparent as significant post-error slowing. P300 data showed that for early HD the No-go amplitude was lower than for the other two groups (p < 0.05). Subjects with early HD showed a reduced capacity to effectively control attention. They proved unable to resume the task directly after having made an error, and need more time to return to pre-error performance levels. No attentional control deficits were found for the premanifest HD group

Evaluating sleep and circadian rhythm disturbances and symptoms of impulsivity and inattention: Implications for adult attention-deficit/hyperactivity disorder

Reports of sleep disturbances and delayed sleep timing in attentiondeficit/ hyperactivity-disorder (ADHD) are common however the aetiology of such features is poorly understood. There is substantial evidence pointing to dysfunction of the circadian timing system in ADHD, and individual differences in human chronotype and diurnal preference have been linked with impulsivity and attention problems in adults. In the work presented here we examined associations between a later circadian phase of entrainment, impaired sleep quality, and circadian misalignment and how they relate to core symptoms of ADHD distributed among the general population. We report novel evidence which suggests that ‘social jetlag’ – an index of circadian misalignment arising from discordance between endogenous circadian timing and the timing of the social clock – is a consistent predictor of poorer ADHD-like symptom outcomes. Furthermore, objective assessment of the rest-activity rhythm and sleep intervals of subjects show that a failure to precisely entrain to the 24 h circadian period is associated with ADHD-like symptom severity which was in turn predicted by delayed circadian phase/sleep phase, sleep quality, and duration. Candidate gene approaches did not replicate previous findings linking symptoms of impulsivity, inattention, and later chronotype with elements of the core molecular clock. However, we did find differential susceptibility to the previously identified risk factors; poor sleep quality and social jetlag which were both modified by genotype. Preliminary data from an exploratory study examining the neurophysiological correlates of response inhibition and selective attention revealed interesting patters of ERP elicitation in individuals with high levels of social jetlag. The current findings highlight how examination of sleep and circadian rhythm disturbances associated with ADHD may inform our understanding of the disorder risk and might in the future be factored into interventions designed for better symptom management

Breaking deadlocks: reward probability and spontaneous preference shape voluntary decisions and electrophysiological signals in humans

Choosing between equally valued options is a common conundrum, for which classical decision theories predicted a prolonged response time (RT). This contrasts with the notion that an optimal decision maker in a stable environment should make fast and random choices, as the outcomes are indifferent. Here, we characterize the neurocognitive processes underlying such voluntary decisions by integrating cognitive modelling of behavioral responses and EEG recordings in a probabilistic reward task. Human participants performed binary choices between pairs of unambiguous cues associated with identical reward probabilities at different levels. Higher reward probability accelerated RT, and participants chose one cue faster and more frequent over the other at each probability level. The behavioral effects on RT persisted in simple reactions to single cues. By using hierarchical Bayesian parameter estimation for an accumulator model, we showed that the probability and preference effects were independently associated with changes in the speed of evidence accumulation, but not with visual encoding or motor execution latencies. Time-resolved MVPA of EEG-evoked responses identified significant representations of reward certainty and preference as early as 120 ms after stimulus onset, with spatial relevance patterns maximal in middle central and parietal electrodes. Furthermore, EEG-informed computational modelling showed that the rate of change between N100 and P300 event-related potentials modulated accumulation rates on a trial-by-trial basis. Our findings suggest that reward probability and spontaneous preference collectively shape voluntary decisions between equal options, providing a mechanism to prevent indecision or random behavior

Cognition in Huntington's disease : the influence of motor behaviour and time

Huntington's disease (HD) is a genetic neurodegenerative disease. Carriers of the HD gene without clinical symptoms of the disease can be identified and studied. The study of these premanifest subjects is of importance for the understanding of preclinical disease progression and for the design of future clinical trials. HD is characterized by progressive decline in motor functioning, cognition and behaviour. The unwanted motor disturbances that patients experience are likely to be of influence on cognitive functioning, as cognitive tests almost always require a motoric response. In this thesis we investigated cognitive functioning in both premanifest HD gene carriers and HD patients by taking into account the motor disturbances that have been reported in both pre- and manifest phases of the disease. We also reports on the influence of time on cognition in HD by means of several longitudinal reports with follow-up periods as long as ten years. We found both carriers and patients deteriorate most on memory and executive functioning domains, with the latter being most sensitive in the premanifest phase. We have also found evidence for the presence of premanifest (cognitive) compensatory mechanisms. As expected, there is a substantial (negative) effect of motor functioning on cognition in HD.de Vereniging van Huntington - Topaz - Lundbeck B.V. - Stichting Alkemade-KeulsUBL - phd migration 201

Akustische Stimulation und deren Einfluss auf neurophysiologische Mechanismen der Fehlerverarbeitung und Fehlerregulation

In dieser Studie wurden 23 Männer zwischen 18 und 30 Jahren in vier Messungen untersucht. Es wurde eine akustische Stimulation mit weißem Rauschen, binauralen Beats und monauralen Beats durchgeführt und parallel eine Verhaltensaufgabe (Go-/NoGo-Aufgabe) absolviert. Zusätzlich wurde ein EEG abgeleitet. Ziel der Studie war es, Mechanismen der Fehlerregulation zu untersuchen und mittels akustischer Stimulation zu beeinflussen