1114 A FUNCTIONAL HOMOLOGY BETWEEN ADHD AND ACUTE SLEEP DEPRIVATION: AN ALE META-ANALYSIS OF FMRI-MONITORED EXECUTIVE FUNCTION

Abstract

Sleep disruption is common in attention deficit hyperactivity disorder (ADHD). Likewise, deficits in executive function are a hallmark of sleep deprivation in healthy individuals. Despite this apparent convergence, whether ADHD and sleep deprivation modulate common, or disparate, neural systems is unknown. While no study has utilized fMRI to investigate sleep loss in ADHD, fMRI is commonly used in sleep deprivation and ADHD independently. Thus, we performed a novel, comparative meta-analysis of fMRI-monitored executive function between sleep deprivation and ADHD. An initial systematic review of task-based fMRI studies of sleep deprivation vs. rested and ADHD vs. controls yielded 126 articles for an activation-likelihood-estimate (ALE) meta-analysis in GingerALE. fMRI coordinates were extracted for each contrast (i.e., “ADHD vs. Controls”, “TSD vs. Rested”) and normalized to the Talairach-atlas. Separate ALE analyses (p < .005) were performed for ADHD and sleep deprivation. These initial estimates were forwarded to conjunction analyses to identify regions where activation was either overlapping or differing significantly between ADHD and sleep deprivation (p < .005; permutation-testing). Conjunction analyses revealed overlapping deactivations between ADHD and sleep loss in central executive-function-regulating regions: dorsal medial anterior cingulate cortex, precentral gyrus, left inferior parietal lobule, and left inferior frontal gyrus. Compared to sleep loss, ADHD was associated with exaggerated hypoactivations within right dorsolateral prefrontal cortex, right anterior insula, and right temporoparietal junction. In contrast, sleep deprivation was associated with significantly exaggerated hyperactivation in subcortical arousal centers, namely, thalamus and striatum. Our study indicates that ADHD and acute sleep deprivation may share a common neural signature: hypoactivation of executive function neuroanatomy. ADHD was associated with exaggerated, but not unique, deactivations in the same network. In contrast, sleep loss exhibited unique hyperactivation in subcortical arousal centers, perhaps intimating a compensatory response in sleep loss not present in ADHD. By elucidating shared from distinct patterns of functional neuroanatomy, these data provide novel targets for future experimental investigations of sleep loss in ADHD. This work was supported by K01MH109854 and T32MH019927.