Task-general efficiency of evidence accumulation as a computationally-defined neurocognitive trait: Implications for clinical neuroscience

Abstract

Quantifying individual differences in higher-order cognitive functions is a foundational area of cognitive science that also has profound implications for research on psychopathology. For the last two decades, the dominant approach in these fields has been to attempt to fractionate higher-order functions into hypothesized components (e.g., “inhibition”, “updating”) through a combination of experimental manipulation and factor analysis. However, the putative structures obtained through this paradigm have recently been met with substantial criticism on both theoretical and empirical grounds. Concurrently, an alternative approach has emerged focusing on parameters of formal computational models of cognition that have been developed in mathematical psychology. These models posit biologically plausible and experimentally validated explanations of the data-generating process for cognitive tasks, allowing them to be used to measure the latent mechanisms that underlie performance. One of the primary insights provided by recent applications of such models is that individual and clinical differences in performance on a wide variety of cognitive tasks, ranging from simple choice tasks to complex executive paradigms, are largely driven by efficiency of evidence accumulation (EEA), a computational mechanism defined by sequential sampling models. This review assembles evidence for the hypothesis that EEA is a central individual difference dimension that explains neurocognitive deficits in multiple clinical disorders and identifies ways in which in this insight can advance clinical neuroscience research. We propose that recognition of EEA as a major driver of neurocognitive differences will allow the field to make clearer inferences about cognitive abnormalities in psychopathology and their links to neurobiology.

Improving the prospective prediction of a near-term suicide attempt in veterans at risk for suicide, using a go/no-go task

“…In electrophysiology studies, decisional efficiency has been linked with the build-up rate of the P3b component of the P300 event-related potential (Kelly & O'Connell, 2013), and appears to originate from temporal-parietal activity associated with stimulus detection and attention (Polich, 2007). Interestingly, reduced decisional efficiency is emerging as a neurocognitive risk factor in a range of psychopathologies (for review, see Weigard & Sripada, 2021). A few studies have suggested that decisional efficiency can be increased by catecholamine agonists that modulate brain signal-to-noise ratios (Peters, Vega, Weinstein, Mitchell, & Kayser, 2020;Weigard, Heathcote, & Sripada, 2019), which may be particularly relevant given that brain serotonergic systems have been associated with suicidality (Oquendo et al, 2014;van Heeringen & Mann, 2014).…”