Date/Time
Date(s) - 09/10/2014
2:00 pm

Cognitive processes refer to high-order mental actions including attention, memory, producing and understanding language, solving problems and making decisions. In this dissertation, we seek to explore the neural representations and mechanisms underlying these cognitive processes through the analyses of electroencephalography (EEG) signals.

First, we applied power and coherence analyses to study the functional role of alpha oscillations in working memory retention. We found that the occipital alpha power and the frontal-occipital alpha coherence increased during memory retention but began to decline before the onset of probe stimulus. Faster reaction time was associated with lower alpha power and lower alpha connectivity. These findings suggest that alpha activity reflects functional inhibition of task-irrelevant brain areas rather than represents memory information. Second, we applied Granger causality analysis to explore the control regions and the neural mechanisms in the top-down modulation of posterior alpha activity. We found that the top-down biasing signals over visual alpha activity are likely mediated by alpha synchrony and issued in a task-specific manner. Third, we applied event-related potential (ERP) analysis to reveal the specific neural cognitive processes evoked by instructional cues in a cued task-switching paradigm. We found four temporally overlapping but functionally and anatomically distinct cue-triggered ERPs, suggesting the neural processes underlying proactive cognitive control are dissociable. Fourth, we studied the effects of cognitive fatigue on behavioral performance. We found that the intraindividual variability of reaction time (RT) increased over time and the increasing slope significantly correlated with the self-report fatigue scales. These findings suggest that the intraindividual variability of RT is a key performance index related to cognitive fatigue. Fifth, we investigated the effects of cognitive fatigue on cue-related neural cognitive processes. We for the first time demonstrated that cognitive compensation is engaged to cope with fatigue induced cognitive impairments and this engagement terminates as cognitive fatigue worsens. Finally, we examined the brain’s response to drug-induced cognitive impairments with respect to the antiepileptic drug topiramate (TPM). We provided the first evidence showing that the brain could employ a compensation mechanism by recruiting more neural resources to cope with the drug-induced impairment under increasing cognitive demand.