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. 2013 May 1:71:275-83.
doi: 10.1016/j.neuroimage.2013.01.025. Epub 2013 Feb 1.

The effects of poor quality sleep on brain function and risk taking in adolescence

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The effects of poor quality sleep on brain function and risk taking in adolescence

Eva H Telzer et al. Neuroimage. .

Abstract

Insufficient sleep and poor quality sleep are pervasive during adolescence and relate to impairments in cognitive control and increased risk taking. However, the neurobiology underlying the association between sleep and adolescent behavior remains elusive. In the current study, we examine how poor sleep quality relates to cognitive control and reward related brain function during risk taking. Forty-six adolescents participated in a functional magnetic imaging (fMRI) scan during which they completed a cognitive control and risk taking task. Behaviorally, adolescents who reported poorer sleep also exhibited greater risk-taking. This association was paralleled by less recruitment of the dorsolateral prefrontal cortex (DLPFC) during cognitive control, greater insula activation during reward processing, and reduced functional coupling between the DLPFC and affective regions including the insula and ventral striatum during reward processing. Collectively, these results suggest that poor sleep may exaggerate the normative imbalance between affective and cognitive control systems, leading to greater risk-taking in adolescents.

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Figures

Fig. 1
Fig. 1
The Go-No-go Task. Participants are shown a letter, presented rapidly with a jittered fixation between each letter trial. Participants push a button as quickly as possible to all letters (Go) except for X (No-go), during which they must withhold the button response.
Fig. 2
Fig. 2
The Balloon Analogue Risk Task. Examples of the three trial types: a) risk-taking trial with an explosion outcome, b) risk-taking trial with a cash-out outcome, and c) control trial in which no money was earned or loss. The trial types used in analyses are depicted in red writing. Note. Pumps on explosion trials and cash-out trials were modeled separately.
Fig. 3
Fig. 3
Percent signal change in right DLPFC to No-go>Go trials that correlated negatively with sleep quality. xyz=30 34 38, Z=3.81, k=441, p<.05 corrected. Note. Right=left. Greater values on the x-axis represent poorer sleep quality. Scatterplots are provided for descriptive purposes. All reported statistics are obtained from independent tests in FSL regressing sleep on brain activation.
Fig. 4
Fig. 4
Percent signal change in the insula during the BART to cash-outs that correlated with poorer sleep quality. xyz=−24 20 −2, Z=3.57, k=711, p<.05, corrected. Note. Right=left. Greater values on the x-axis represent poorer sleep quality. Scatterplots are provided for descriptive purposes. All reported statistics are obtained from independent tests in FSL regressing sleep on brain activation.
Fig. 5
Fig. 5
(a) the seed region was defined as a 6 mm sphere centered in the DLPFC from the cluster that correlated with sleep quality during the GNG. (b) Psychophysiological interaction analyses reveal less functional coupling between the DLPFC and neural regions for adolescents with poorer sleep quality. (c) Percent signal change in the insula and ventral striatum that showed decreased functional coupling with the DLPFC that correlated negatively with sleep quality. Note, greater values on the x-axis represent poorer sleep quality. Note. Right=left. Scatterplots are provided for descriptive purposes. All reported statistics are obtained from independent tests in FSL regressing sleep on brain activation.

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