Sleep deprivation reduces default mode network connectivity and anti-correlation during rest and task performance.

Sleep deprivation (SD) can alter extrinsic, task-related fMRI signal involved in attention, memory and executive function. However, its effects on intrinsic low-frequency connectivity within the Default Mode Network (DMN) and its related anti-correlated network (ACN) have not been well characterized. We investigated the effect of SD on functional connectivity within the DMN, and on DMN-ACN anti-correlation, both during the resting state and during performance of a visual attention task (VAT). 26 healthy participants underwent fMRI twice: once after a normal night of sleep in rested wakefulness (RW) and once following approximately 24h of total SD. A seed-based approach was used to examine pairwise correlations of low-frequency fMRI signal across different nodes in each state. SD was associated with significant selective reductions in DMN functional connectivity and DMN-ACN anti-correlation. This was congruent across resting state and VAT analyses, suggesting that SD induces a robust alteration in the intrinsic connectivity within and between these networks.

Effects of sleep deprivation on cortical activation during directed attention in the absence and presence of visual stimuli.

Sleep deprivation (SD) can give rise to faltering attention but the mechanics underlying this remain uncertain. Using a covert attention task that required attention to a peripheral target location, we compared the effects of attention and SD on baseline activity prior to visual stimulation as well as on stimulus-evoked activity. Volunteers were studied after a night of normal sleep (RW) and a night of SD. Baseline signal elevations evoked by preparatory attention in the absence of visual stimulation were attenuated within rFEF, rIPS (sparing SEF) and all retinotopically mapped visual areas during SD, indicative of impaired endogenous attention. In response to visual stimuli, attention modulated activation in higher cortical areas and extrastriate cortex (hV4, ventral occipital areas) after RW. SD attenuated rFEF, rIPS, V3a and VO stimulus-evoked activation regardless of whether stimuli were attended. Notably, the modulation of stimulus-evoked activation by attention was not affected by SD unlike for the preparatory period, suggesting a reduced number, but still functional circuits during SD. Deficits in endogenous attention in SD dominate in the preparatory period, whereas changes in stimulus-related activation arise from an interaction between compromised fronto-parietal top-down control of attention and reduced sensitivity of extrastriate visual cortex to top-down or bottom-up inputs.

Sleep deprivation and interference by emotional distracters.

STUDY OBJECTIVES: We determined if sleep deprivation would amplify the effect of negative emotional distracters on working memory. DESIGN: A crossover design involving 2 functional neuroimaging scans conducted at least one week apart. One scan followed a normal night of sleep and the other followed 24 h of sleep deprivation. Scanning order was counterbalanced across subjects. SETTING: The study took place in a research laboratory. PARTICIPANTS: 24 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Study participants were scanned while performing a delayed-response working memory task. Two distracters were presented during the maintenance phase, and these differed in content: highly arousing, negative emotional scenes; low-arousing, neutral scenes; and digitally scrambled versions of the pictures. Irrespective of whether volunteers were sleep deprived, negative emotional (relative to neutral) distracters elicited greater maintenance-related activity in the amygdala, ventrolateral prefrontal cortex, and fusiform gyri, while concurrently depressing activity in cognitive control regions. Individuals who maintained or increased distracter-related amygdala activation after sleep deprivation showed increased working memory disruptions by negative emotional distracters. These individuals also showed reduced functional connectivity between the amygdala and the ventromedial and dorsolateral prefrontal cortices, regions postulated to mediate cognitive control against emotional distraction. CONCLUSIONS: Increased distraction by emotional stimuli following sleep deprivation is accompanied by increases in amygdala activation and reduced functional connectivity between the amygdala and prefrontal cognitive control regions. These findings shed light on the neural basis for interindividual variation in how negative emotional stimuli might distract sleep deprived persons.

Sleep deprivation impairs object-selective attention: a view from the ventral visual cortex.

BACKGROUND: Most prior studies on selective attention in the setting of total sleep deprivation (SD) have focused on behavior or activation within fronto-parietal cognitive control areas. Here, we evaluated the effects of SD on the top-down biasing of activation of ventral visual cortex and on functional connectivity between cognitive control and other brain regions. METHODOLOGY/PRINCIPAL FINDINGS: Twenty-three healthy young adult volunteers underwent fMRI after a normal night of sleep (RW) and after sleep deprivation in a counterbalanced manner while performing a selective attention task. During this task, pictures of houses or faces were randomly interleaved among scrambled images. Across different blocks, volunteers responded to house but not face pictures, face but not house pictures, or passively viewed pictures without responding. The appearance of task-relevant pictures was unpredictable in this paradigm. SD resulted in less accurate detection of target pictures without affecting the mean false alarm rate or response time. In addition to a reduction of fronto-parietal activation, attending to houses strongly modulated parahippocampal place area (PPA) activation during RW, but this attention-driven biasing of PPA activation was abolished following SD. Additionally, SD resulted in a significant decrement in functional connectivity between the PPA and two cognitive control areas, the left intraparietal sulcus and the left inferior frontal lobe. CONCLUSIONS/SIGNIFICANCE: SD impairs selective attention as evidenced by reduced selectivity in PPA activation. Further, reduction in fronto-parietal and ventral visual task-related activation suggests that it also affects sustained attention. Reductions in functional connectivity may be an important additional imaging parameter to consider in characterizing the effects of sleep deprivation on cognition.

Sleep deprivation and its effects on object-selective attention.

Sleep deprivation (SD) affects attention but it is an open question as to whether all subtypes of attention are similarly affected. We investigated the effects of 24 h of total SD on object-selective attention. 26 healthy, young adults viewed quartets of alternating faces or place scenes and performed selective judgments on faces only, scenes only or both faces and scenes. Volunteers underwent fMRI following a normal night of sleep and again following approximately 24 h of total sleep deprivation in a counterbalanced fashion. Sleep deprivation resulted in slower and less accurate picture classification as well as poorer recognition memory for scenes. Attention strongly modulated activation in the Parahippocampal Place Area (PPA). Task-related activation in the fronto-parietal cortex and PPA was reduced in SD, but the relative modulation of PPA activation by attention was preserved. Psychophysiological interaction between the left intra-parietal sulcus and the PPA that was clearly present after a normal night of sleep was reduced below threshold following SD suggesting that PPI may be a more sensitive method of detecting change in selective attention. Sleep deprivation may affect object-selective attention in addition to exerting a task-independent deficit in attention.

Lapsing during sleep deprivation is associated with distributed changes in brain activation.

Lapses of attention manifest as delayed behavioral responses to salient stimuli. Although they can occur even after a normal night's sleep, they are longer in duration and more frequent after sleep deprivation (SD). To identify changes in task-associated brain activation associated with lapses during SD, we performed functional magnetic resonance imaging during a visual, selective attention task and analyzed the correct responses in a trial-by-trial manner modeling the effects of response time. Separately, we compared the fastest 10% and slowest 10% of correct responses in each state. Both analyses concurred in finding that SD-related lapses differ from lapses of equivalent duration after a normal night's sleep by (1) reduced ability of frontal and parietal control regions to raise activation in response to lapses, (2) dramatically reduced visual sensory cortex activation, and (3) reduced thalamic activation during lapses that contrasted with elevated thalamic activation during nonlapse periods. Despite these differences, the fastest responses after normal sleep and after SD elicited comparable frontoparietal activation, suggesting that performing a task while sleep deprived involves periods of apparently normal neural activation interleaved with periods of depressed cognitive control, visual perceptual functions, and arousal. These findings reveal for the first time some of the neural consequences of the interaction between efforts to maintain wakefulness and processes that initiate involuntary sleep in sleep-deprived persons.