Vigilance behaviors and EEG activity in sustained attention may affect acute pain

Chien, JH; Korzeniewska, A; Hillis, AE; Kim, JH; Emerson, N; Greenspan, JD; Campbell, CM; Meeker, TJ; Markman, TM; Lenz, FA · 2017 · Crossref

DOI: 10.15761/jsin.1000184

archive: archived pipeline: cataloged verified

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Summary

This study investigates the neural mechanisms underlying sustained attention to acute pain, addressing a gap in literature where sustained attention has been extensively studied for visual, auditory, and somatic stimuli but rarely for painful stimuli. The researchers hypothesized that sustained attention to pain would induce a "vigilance decrement"—a decrease in neural activity and increase in errors over time—and that Beta band Event-Related Spectral Perturbation (ERSP) would correlate with performance errors. The experimental design involved sixteen healthy participants performing a Continuous Performance Task (CPT). Subjects were instructed to count painful laser stimuli (targets) presented randomly among nonpainful electrical stimuli (nontargets) during prolonged blocks. Scalp EEG was recorded to measure ERSP, defined as the ratio of post-stimulus oscillatory power to baseline power. The analysis focused on four specific time-frequency windows: early Delta/Theta (0–8 Hz), late Delta/Theta (0–8 Hz), Alpha (8–14 Hz), and Beta (14–30 Hz). Performance was quantified by error rates, defined as the discrepancy between counted and actual target stimuli. The results confirmed the presence of a vigilance decrement, with error rates increasing significantly in the second interval of the task compared to the first. This increase in errors was inversely correlated with laser energy, pain unpleasantness, and stimulus salience. Regarding EEG activity, the Alpha ERSP decreased over time on task, while Beta ERSP increased. Crucially, higher error rates were directly correlated with increased Beta ERS in central scalp channels. Additionally, subjects with high error rates exhibited distinct ERSP patterns compared to low-error subjects, including higher Beta ERS and altered Delta/Theta responses. The findings suggest that sustained attention to pain modulates pain sensation through specific oscillatory changes in frontoparietal networks. The observed sequence of decreased Alpha ERD followed by increased Beta ERS likely reflects a shift from cortical excitation to inhibition. The correlation between Beta activity and errors implies that parietal cortex activity is integral to maintaining vigilance and detecting painful stimuli. These results provide novel evidence that neural activity associated with sustained attention deficits may mediate the experience of acute pain, suggesting that parietal cortex dysfunction could be a target for treating pain syndromes characterized by hypervigilance.

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