Optimal multisensory decision-making in a reaction-time task
Abstract
Humans and animals can integrate sensory evidence from various sources to make decisions in a statistically near-optimal manner, provided that the stimulus presentation time is fixed across trials. Little is known about whether optimality is preserved when subjects can choose when to make a decision (reaction-time task), nor when sensory inputs have time-varying reliability. Using a reaction-time version of a visual/vestibular heading discrimination task, we show that behavior is clearly sub-optimal when quantified with traditional optimality metrics that ignore reaction times. We created a computational model that accumulates evidence optimally across both cues and time, and trades off accuracy with decision speed. This model quantitatively explains subjects' choices and reaction times, supporting the hypothesis that subjects do, in fact, accumulate evidence optimally over time and across sensory modalities, even when the reaction time is under the subject's control.
Article and author information
Author details
Ethics
Human subjects: Informed consent was obtained from all participants and all procedures were reviewed and approved by the Washington University Office of Human Research Protections (OHRP), Institutional Review Board (IRB; IRB ID# 201109183). Consent to publish was not obtained in writing, as it was not required by the IRB, but all subjects were recruited for this purpose and approved verbally. Of the initial seven subjects, three participated in a follow-up experiment roughly two years after the initial data collection. Procedures for the follow-up experiment were approved by the Institutional Review Board for Human Subject Research for Baylor College of Medicine and Affiliated Hospitals (BCM IRB, ID# H-29411) and informed consent and consent to publish was given again by all three subjects.
Copyright
© 2014, Drugowitsch et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 6,568
- views
-
- 893
- downloads
-
- 101
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Immunology and Inflammation
- Neuroscience
Somatic genetic heterogeneity resulting from post-zygotic DNA mutations is widespread in human tissues and can cause diseases, however, few studies have investigated its role in neurodegenerative processes such as Alzheimer’s disease (AD). Here, we report the selective enrichment of microglia clones carrying pathogenic variants, that are not present in neuronal, glia/stromal cells, or blood, from patients with AD in comparison to age-matched controls. Notably, microglia-specific AD-associated variants preferentially target the MAPK pathway, including recurrent CBL ring-domain mutations. These variants activate ERK and drive a microglia transcriptional program characterized by a strong neuro-inflammatory response, both in vitro and in patients. Although the natural history of AD-associated microglial clones is difficult to establish in humans, microglial expression of a MAPK pathway activating variant was previously shown to cause neurodegeneration in mice, suggesting that AD-associated neuroinflammatory microglial clones may contribute to the neurodegenerative process in patients.
-
- Neuroscience
Historically, the creation of the parasympathetic division of the autonomic nervous system of the vertebrates is inextricably linked to the unification of the cranial and sacral autonomic outflows. There is an intriguing disproportion between the entrenchment of the notion of a ‘cranio-sacral’ pathway, which informs every textbook schematic of the autonomic nervous system since the early XXth century, and the wobbliness of its two roots: an anatomical detail overinterpreted by Walter Holbrook Gaskell (the ‘gap’ between the lumbar and sacral outflows), on which John Newport Langley grafted a piece of physiology (a supposed antagonism of these two outflows on external genitals), repeatedly questioned since, to little avail. I retrace the birth of a flawed scientific concept (the cranio-sacral outflow) and the way in which it ossified instead of dissipated. Then, I suggest that the critique of the ‘cranio-sacral outflow’ invites, in turn, a radical deconstruction of the very notion of a ‘parasympathetic’ outflow, and a more realistic description of the autonomic nervous system.