Acute Stress Effects on Executive Function
Meta-analysis (Shields, Sazma, & Yonelinas 2016) across 51 studies: Acute stress impaired working memory (g+ = -0.20, p = .005), cognitive flexibility (g+ = -0.30, p = .039), and cognitive inhibition (g+ = -0.208, p = .021), while enhancing response inhibition.
Key moderators
- Working memory impairment greater at high cognitive load (g+ = -0.303, p = .005) and with greater delay from stress onset
- Male participants showed greater impairment
- Social stressors produced significant effects; pain stressors did not reach significance
Critical finding
Stress effects differed markedly from cortisol administration effects, indicating stress works through mechanisms beyond cortisol alone -- consistent with the catecholamine-PFC mechanism (Arnsten).
Effects increase rather than decrease with delay from stress onset (B = -0.006, p = .044), which is the opposite of cortisol administration effects and consistent with catecholamine-mediated mechanisms.
Architectural implication
"Stress contributes to a cognitive state of reactive and automatic processing while also enhancing executive motor control" -- the brain shifts to a mode that facilitates engagement with or escape from the current stressor, at the cost of higher cognitive functions. This is exactly the state where the human cannot access their own evaluative processes.
Source verification
Shields, Sazma, & Yonelinas 2016 (Neurosci. Biobehav. Rev. 68:651-668) -- verified.