Most computational theories of cognition lack a representation of physiology. Understanding the cognitive effects of compounds present in the environment is important for explaining and predicting changes in cognition and behavior given exposure to toxins, pharmaceuticals, or the deprivation of critical compounds like oxygen. This research integrates physiologically based pharmacokinetic (PBPK) model predictions of caffeine concentrations in blood and tissues with ACT-R's fatigue module to predict the effects of caffeine on fatigue. Mapping between the PBPK model parameters and ACT-R model (...) parameters is informed by the neurophysiological literature and established associations between ACT-R modules and brain regions. The results from three such parameter mappings are explored to explain observed data from sleep-deprived participants performing the psychomotor vigilance test with and without caffeine. Predicted caffeine concentrations in the brain are used to modulate procedural parameters in the fatigue module to explain caffeine's effects on multiple performance metrics. (shrink)

Veksler and Gunzelmann argue that the vigilance decrement and the deleterious effects of sleep loss reflect functionally equivalent degradations in cognitive processing and performance. Our account is implemented in a cognitive architecture, where these factors produce breakdowns in goal-directed cognitive processing that we refer to as microlapses. Altmann raises a number of challenges to microlapses as a unified account of these deficits. Under scrutiny, however, the challenges do little to discredit the theory or conclusions in the original paper. In our (...) response, we address the most serious challenges. In so doing, we provide additional support for the theory and mechanisms, and we highlight opportunities for extending their explanatory breadth. (shrink)

Veksler and Gunzelmann make an extraordinary claim, which is that sleep deprivation effects and the vigilance decrement are functionally equivalent. Extraordinary claims require extraordinary evidence, which is missing from Veksler and Gunzelmann's study. Their behavioral data offer only weak theoretical constraint, and to the extent their modeling exercise supports any position, it is that these two performance impairments involve functionally distinct underlying mechanisms.