The authors stratify post-COVID participants based on the number of “brain fog” symptoms reported using the DePaul Symptom Questionnaire (DSQ), a subjective tool originally designed for chronic fatigue syndrome, and then relate the severity of those reported symptoms to differences in posterior alpha rsEEG source activity.
However, this introduces a key conceptual and methodological concern: The same subjective perception of chronic fatigue that defines the BF+ subgroup also likely correlates with reduced arousal or vigilance, both of which are known to influence posterior alpha activity during eyes-closed EEG. Thus, is it valid to conclude that reduced alpha activity reflects a brain-level “marker” of post-COVID brain fog, when symptom grouping is based on fatigue, and fatigue itself modulates alpha rhythms?
In other words, there’s a risk of circular inference: Individuals are grouped based on a fatigue-centric questionnaire,
Alpha attenuation, which is known to co-vary with fatigue and drowsiness, is then interpreted as a neurophysiological marker of the very construct (fatigue) used for grouping.
Furthermore, although the authors mention vigilance monitoring during EEG recordings, there is no objective measure of vigilance/arousal state (e.g., reaction time tasks, pupillometry, or independent EEG drowsiness classifiers) reported to disentangle alpha changes driven by trait neurobiology vs. state-related mental fatigue.
How do the authors account for the confounding effect of arousal state or momentary vigilance during EEG recordings, especially when both the grouping (via DSQ fatigue symptoms) and the primary finding (posterior alpha suppression) may stem from the same physiological process? Could this reduce the specificity of posterior alpha suppression as a marker for post-COVID neurophysiological alteration, rather than simply reflecting acute fatigue state?