Alpha oscillations (8–12 Hz) are thought to inversely correlate with cortical excitability. Goal-oriented modulation of alpha has been studied extensively. In visual spatial attention, alpha over the region of visual cortex corresponding to the attended location decreases, signifying increased excitability to facilitate the processing of impending stimuli. In contrast, in retention of verbal working memory, alpha over visual cortex increases, signifying decreased excitability to gate out stimulus input to protect the information held online from sensory interference. According to the prevailing model, this goal-oriented biasing of sensory cortex is effected by top-down control signals from frontal and parietal cortices. The present study tests and substantiates this hypothesis by (a) identifying the signals that mediate the top-down biasing influence, (b) examining whether the cortical areas issuing these signals are task-specific or task-independent, and (c) establishing the possible mechanism of the biasing action. High-density human EEG data were recorded in two experimental paradigms: a trial-by-trial cued visual spatial attention task and a modified Sternberg working memory task. Applying Granger causality to both sensor-level and source-level data we report the following findings. In covert visual spatial attention, the regions exerting top-down control over visual activity are lateralized to the right hemisphere, with the dipoles located at the right frontal eye field (FEF) and the right inferior frontal gyrus (IFG) being the main sources of top-down influences. During retention of verbal working memory, the regions exerting top-down control over visual activity are lateralized to the left hemisphere, with the dipoles located at the left middle frontal gyrus (MFG) being the main source of top-down influences. In both experiments, top-down influences are mediated by alpha oscillations, and the biasing effect is likely achieved via an inhibition-disinhibition mechanism.

Prolonged continuous performance of a cognitively demanding task induces cognitive fatigue and is associated with a time-related deterioration of objective performance, the degree of which is referred to cognitive fatigability. Although the neural underpinnings of cognitive fatigue are poorly understood, prior studies report changes in neural activity consistent with deterioration of task-related networks over time. While compensatory brain activity is reported to maintain motor task performance in the face of motor fatigue and cognitive performance in the face of other stressors (e.g., aging) and structural changes, there are no studies to date demonstrating compensatory activity for cognitive fatigue. High-density electroencephalography was recorded from human subjects during a 160 min continuous performance of a cognitive control task. While most time-varying neural activity showed a linear decline over time, we identified an evoked potential over the anterior frontal region which demonstrated an inverted U-shaped time-on-task profile. This evoked brain activity peaked between 60 and 100 min into the task and was positively associated with better behavioral performance only during this interval. Following the peak and during subsequent decline of this anterior frontal activity, the rate of performance decline also accelerated. These findings demonstrate that this anterior frontal brain activity, which is not part of the primary task-related activity at baseline, is recruited to compensate for fatigue-induced impairments in the primary task-related network, and that this compensation terminates as cognitive fatigue further progresses. These findings may be relevant to understanding individual differences in cognitive fatigability and developing interventions for clinical conditions afflicted by fatigue.

Cognitive fatigability is conventionally quantified as the increase over time in either mean reaction time (RT) or error rate from two or more time periods during sustained performance of a prolonged cognitive task. There is evidence indicating that these mean performance measures may not sufficiently reflect the response characteristics of cognitive fatigue. We hypothesized that changes in intraindividual variability over time would be a more sensitive and ecologically meaningful metric for investigations of fatigability of cognitive performance. To test the hypothesis fifteen young adults were recruited. Trait fatigue perceptions in various domains were assessed with the Multidimensional Fatigue Index (MFI). Behavioral data were then recorded during performance of a three-hour continuous cued Stroop task. Results showed that intraindividual variability, as quantified by the coefficient of variation of RT, increased linearly over the course of three hours and demonstrated a significantly greater effect size than mean RT or accuracy. Change in intraindividual RT variability over time was significantly correlated with relevant subscores of the MFI including reduced activity, reduced motivation and mental fatigue. While change in mean RT over time was also correlated with reduced motivation and mental fatigue, these correlations were significantly smaller than those associated with intraindividual RT variability. RT distribution analysis using an ex-Gaussian model further revealed that change in intraindividual variability over time reflects an increase in the exponential component of variance and may reflect attentional lapses or other breakdowns in cognitive control. These results suggest that intraindividual variability and its change over time provide important metrics for measuring cognitive fatigability and may prove useful for inferring the underlying neuronal mechanisms of both perceptions of fatigue and objective changes in performance.

Mild traumatic brain injury (mTBI) has been firmly associated with disrupted white matter integrity due to induced white matter damage and degeneration. However, comparatively less is known about the changes of the intrinsic functional connectivity mediated via neural synchronization in the brain after mTBI. Moreover, despite the presumed link between structural and functional connectivity, no existing studies in mTBI have demonstrated clear association between the structural abnormality of white matter axons and the disruption of neural synchronization. To investigate these questions, we recorded resting state EEG and diffusion tensor imaging (DTI) from a cohort of military service members. A newly developed synchronization measure, the weighted phase lag index was applied on the EEG data for estimating neural synchronization. Fractional anisotropy was computed from the DTI data for estimating white matter integrity. Fifteen service members with a history of mTBI within the past 3 years were compared to 22 demographically similar controls who reported no history of head injury. We observed that synchronization at low-gamma frequency band (25–40 Hz) across scalp regions was significantly decreased in mTBI cases compared with controls. The synchronization in theta (4–7 Hz), alpha (8–13 Hz), and beta (15–23 Hz) frequency bands were not significantly different between the two groups. In addition, we found that across mTBI cases, the disrupted synchronization at low-gamma frequency was significantly correlated with the white matter integrity of the inferior cerebellar peduncle, which was also significantly reduced in the mTBI group. These findings demonstrate an initial correlation between the impairment of white matter integrity and alterations in EEG synchronization in the brain after mTBI. The results also suggest that disruption of intrinsic neural synchronization at low-gamma frequency may be a characteristic functional pathology following mTBI and may prove useful for developing better methods of diagnosis and treatment.

Asymmetrical activation of right and left hemispheres differentially influences the autonomic nervous system. Additionally, each hemisphere primarily receives retinocollicular projections from the contralateral eye. To learn if asymmetrical hemispheric activation induced by monocular viewing would influence relative pupillary size and respiratory hippus variability (RHV), a measure of parasympathetic activity, healthy participants had their left, right or neither eye patched. Pupillary sizes were then recorded with infrared pupillography. Pupillary dilation was significantly greater with left than right eye viewing. RHV, however, was not different between eye viewing conditions. These differences in pupil dilatation may have been caused by relatively greater activation of the right hemispheric-mediated sympathetic activity induced by left monocular viewing or relatively greater deactivation of the left hemispheric-mediated parasympathetic activity induced by right eye patching. The absence of an asymmetry in RHV, however, suggests that hemispheric asymmetry of sympathetic activation was primarily responsible for this ocular asymmetry of pupil dilation.