Abstract

Prolonged performance of a demanding cognitive task induces cognitive fatigue. We examined the behavioral and neural responses to fatigue-induced cognitive impairments in young and older adults. Particular emphasis was placed on whether the brain exhibited compensatory neural activity in response to cognitive fatigue. High-density EEG was recorded from a young (n = 16; 18–33 years of age) and an older (n = 18; 60–87 years of age) cohort who performed a Stroop task continuously for ∼2 h with no breaks. In the young cohort, behavioral performance declined as the experiment progressed, reflecting the deleterious effects of cognitive fatigue. Neurophysiologically, in addition to declining neural activity as cognitive fatigue developed, there is also evidence of region- and time-specific increase in neural activity, suggesting neural compensation. The compensatory activities followed patterns paralleling that of posterior-anterior shift in aging (PASA) and early to late shift in aging (ELSA) observed in cognitive aging and helped to moderate fatigue-induced behavioral deterioration. In the older cohort, behavioral performance did not decline as the experiment progressed, and neural activity either declined or stayed unchanged, showing no evidence of neural compensation, in contrast to the young. These results suggest that young and older adults coped with cognitive fatigue differently by exhibiting differential responses as a function of time-on-task at both the behavioral level and the neural level.

Highlights

  • Compared to the appropriate control groups, cognition is generally impaired in the aged population and in patients suffering from neurological diseases

  • In the subsequent analysis we mainly focused on the change in coefficient of variation of reaction time (CVRT) because CVRT has been shown to be a good behavioral measure for characterizing cognitive fatigue (Wang et al, 2014)

  • Whereas late event-related potentials (ERP) components in occipital-temporal regions of interest (ROIs) decreased with increase in time-ontask, late ERP components in the central-frontal ROI increased with increase in time-on-task, suggesting posterior impairments of neural processing that were accompanied by frontal neural compensation

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Summary

Introduction

Compared to the appropriate control groups, cognition is generally impaired in the aged population and in patients suffering from neurological diseases. Task-evoked neural responses in the aging or diseased brain are generally weaker, signifying impaired brain function (Carter et al, 2001; Lorist et al, 2005; Cader et al, 2006; Cheng and Hsu, 2011). Studies have found brain regions where the activation is stronger in aging and in neurological diseases, and these increased activities are thought to reflect neural compensation (Cabeza et al, 2002); the neural networks associated with these compensatory activities are termed. Posterioranterior shift in aging (PASA) reflects that impaired posterior sensory processing is associated with increased compensatory activity in higher-order anterior brain areas (Cabeza et al, 2004). To late shift in aging (ELSA), observed in age-related impairments during working memory tasks, reflects a reduction in brain activity during an early period of neural processing (e.g., memory retention), which is followed by increase in brain activity in a later period of neural processing (e.g., memory retrieval) (Dew et al, 2012)

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