These results suggest that sleep deprivation poses a dual threat to competent decision making by modulating activation in nucleus accumbens and insula, brain regions associated with risky decision making and emotional processing.

Sleep deprivation results in the loss of our ability to suppress a prepotent response. The extent of decline in this executive function varies across individuals. Here, we used functional magnetic resonance imaging to study the neural correlates of sleep deprivation-induced differences in inhibitory efficiency. Participants performed a go/no-go task after normal sleep and after 24 h of total sleep deprivation. Regardless of the extent of change in inhibitory efficiency, sleep deprivation lowered go/no-go sustained, task-related activation of the ventral and anterior prefrontal (PFC) regions bilaterally. However, individuals better able to maintain inhibitory efficiency after sleep deprivation could be distinguished by lower stop-related, phasic activation of the right ventral PFC during rested wakefulness. These persons also showed a larger rise in such activation both here and in the right insula after sleep deprivation relative to those whose inhibitory efficiency declined.

Sleep deprivation (SD) impairs short-term memory, but it is unclear whether this is because of reduced storage capacity or processes contributing to appropriate information encoding. We evaluated 30 individuals twice, once after a night of normal sleep and again after 24 h of SD. In each session, we evaluated visual memory capacity by presenting arrays of one to eight colored squares. Additionally, we measured cortical responses to varying visual array sizes without engaging memory. The magnitude of intraparietal sulcus activation and memory capacity after normal sleep were highly correlated. SD elicited a pattern of activation in both tasks, indicating that deficits in visual processing and visual attention accompany and could account for loss of short-term memory capacity. Additionally, a comparison between better and poorer performers showed that preservation of precuneus and temporoparietal junction deactivation with increasing memory load corresponds to less performance decline when one is sleepdeprived.attention ͉ extrastriate cortex ͉ parietal cortex ͉ functional MRI ͉ fatigue A ir or ship traffic control and long-distance driving, as well as patient status monitoring in intensive care units, are examples where failure to detect, register, and process visual information as a result of sleep deprivation (SD) may have disastrous outcomes. One of the bottlenecks constraining visual information processing is the capacity to capture and briefly retain items in visual short-term memory (VSTM) to detect behaviorally salient events (1).VSTM capacity is limited to approximately four easily discriminated objects (2, 3). The neural substrate for temporary storage of visual information has been localized to the parietal lobes (4). When VSTM is deliberately engaged, the intraparietal sulcus (IPS) in both hemispheres shows a monotonic increase in activation corresponding to set size until memory capacity is reached, whereupon activation asymptotes. When the same arrays are viewed without having to remember the constituent elements, parietal activation is insensitive to perceptual load. In contrast, activation in the extrastriate visual region is sensitive to perceptual load, increasing monotonically with increasing set size (at least up to a set size of eight). These observations provide dissociable regions to examine the neural substrates of storage capacity and perceptual load.The response of posterior cortical regions to SD is of interest, because prior experiments involving verbal short-term memory in the context of SD have consistently shown reduced taskrelated activation in the parietal cortex (5-8). This decline in activation has been shown to reliably correlate with the extent of performance decline in verbal short-term memory after SD. Additionally, we found that of various metrics, response-time variability best correlated with SD-related reduction in posterior parietal activation (9). This suggests that degraded attention rather than loss of storage capacity per se may account for the observed changes in bra...