The Adolescent Brain Cognitive Development (ABCD) study is an unprecedented longitudinal neuroimaging sample that tracks the brain development of over 10,000 9-10 year olds through adolescence. At the core of this study are the three tasks that are completed repeatedly within the MRI scanner, one of which is the stop-signal task. In analyzing the available stopping experimental code and data, we identified a set of design issues that we believe significantly compromise its value. These issues include but are not limited to: variable stimulus durations that violate basic assumptions of dominant stopping models, trials in which stimuli are incorrectly not presented, and faulty stop-signal delays. We present eight issues, show their effect on the existing ABCD data, suggest prospective solutions including task changes for future data collection and preliminary computational models, and suggest retrospective solutions for data users who wish to make the most of the existing data.
The ABCD dataset is openly available through the NIH Data Archive (https://nda.nih.gov/abcd). Analysis code is available at: http://doi.org/10.5281/zenodo.4458428 and http://doi.org/10.5281/zenodo.4458767.
Adolescent Brain Cognitive Development [ABCD]NIMH Data Archive Collection #2573.
The authors declare that there was no funding for this work.
- Birte U Forstmann, University of Amsterdam, Netherlands
© 2021, Bissett 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.
Cochlear implants are neuroprosthetic devices that can restore hearing in people with severe to profound hearing loss by electrically stimulating the auditory nerve. Because of physical limitations on the precision of this stimulation, the acoustic information delivered by a cochlear implant does not convey the same level of acoustic detail as that conveyed by normal hearing. As a result, speech understanding in listeners with cochlear implants is typically poorer and more effortful than in listeners with normal hearing. The brain networks supporting speech understanding in listeners with cochlear implants are not well understood, partly due to difficulties obtaining functional neuroimaging data in this population. In the current study, we assessed the brain regions supporting spoken word understanding in adult listeners with right unilateral cochlear implants (n=20) and matched controls (n=18) using high-density diffuse optical tomography (HD-DOT), a quiet and non-invasive imaging modality with spatial resolution comparable to that of functional MRI. We found that while listening to spoken words in quiet, listeners with cochlear implants showed greater activity in the left prefrontal cortex than listeners with normal hearing, specifically in a region engaged in a separate spatial working memory task. These results suggest that listeners with cochlear implants require greater cognitive processing during speech understanding than listeners with normal hearing, supported by compensatory recruitment of the left prefrontal cortex.
Sleep strongly affects synaptic strength, making it critical for cognition, especially learning and memory formation. Whether and how sleep deprivation modulates human brain physiology and cognition is not well understood. Here we examined how overnight sleep deprivation vs overnight sufficient sleep affects (a) cortical excitability, measured by transcranial magnetic stimulation, (b) inducibility of long-term potentiation (LTP)- and long-term depression (LTD)-like plasticity via transcranial direct current stimulation (tDCS), and (c) learning, memory, and attention. The results suggest that sleep deprivation upscales cortical excitability due to enhanced glutamate-related cortical facilitation and decreases and/or reverses GABAergic cortical inhibition. Furthermore, tDCS-induced LTP-like plasticity (anodal) abolishes while the inhibitory LTD-like plasticity (cathodal) converts to excitatory LTP-like plasticity under sleep deprivation. This is associated with increased EEG theta oscillations due to sleep pressure. Finally, we show that learning and memory formation, behavioral counterparts of plasticity, and working memory and attention, which rely on cortical excitability, are impaired during sleep deprivation. Our data indicate that upscaled brain excitability and altered plasticity, due to sleep deprivation, are associated with impaired cognitive performance. Besides showing how brain physiology and cognition undergo changes (from neurophysiology to higher-order cognition) under sleep pressure, the findings have implications for variability and optimal application of noninvasive brain stimulation.