Abstract
Classic psychedelics such as psilocybin and LSD are known to acutely disrupt executive function, producing impairments in response inhibition, working memory, and cognitive flexibility. Paradoxically, these compounds often lead to lasting improvements in cognitive flexibility, insight, and goal-directed behavior in the days and weeks following administration. This apparent contradiction has traditionally been interpreted as a biphasic modulation of control capacity—initial impairment followed by compensatory enhancement.An alternative account is proposed in the PRISM model (Psychedelic Recalibration of Internal Salience and Mental Effort Costs), which reframes cognitive outcomes not as shifts in capacity, but as changes in motivation for cognitive control. According to this framework, psychedelics may reduce the perceived cost of cognitive effort during acute states by disrupting habitual internally directed processes, such as Default Mode Network activity. Post-acutely, increased salience of emotionally or personally meaningful goals may enhance the willingness to engage in effortful, goal-directed cognition.Rather than a global increase in executive ability, observed changes in performance may reflect a dynamic reallocation of motivational resources, explaining both acute dissociations and post-acute improvements in specific cognitive domains. This model integrates recent behavioral, neuroimaging, and pharmacological findings to offer testable predictions for future research. New experimental paradigms are outlined for dissociating motivational engagement from cognitive capacity, providing a mechanistic bridge between subjective psychedelic experiences and enduring adaptive outcomes.