Effects of sleep deprivation

Sleep deprivation (SD) is a fairly common event that can be experienced sporadically (e.g. following traumatic events or periods of high stress) or chronically (e.g. living in a noisy environment or working under an irregular schedule) [8]. SD is also a leading cause of serious accidents, for instance at work or while driving, which can result in injuries or death [50,143]. While it is established that SD results in impaired cognitive functions, the effects of SD on waking brain activity are still largely unknown. However, several recent neuroimaging studies have begun addressing this issue. Specifically, these studies have investigated with imaging scans the cognitive functions of sleep-deprived healthy subjects, in order to identify the neuroanatomical correlates of both impaired cognitive performance and of possible compensatory mechanisms. The cognitive domains most characterized include working memory [144-150] and attention [151-153]. Other cognitive aspects, including inhibitory control [154] and emotional processing [155], have also been explored.

Working memory (WM) requires temporarily storing and manipulating information in specific brain areas. Neuroimaging studies have consistently shown an involvement of dorsolateral prefrontal [156] and parietal cortices [157] during WM tasks. However, the

Figure 3.5 Corticalplasticity is reflected by localchanges in SWA. In each panel regions with SWA increase are in red, while in blue are regions with SWA decrease. White circles indicate electrodes with significant SWA activity change. (a) Increased SWA after a rotation learning task. Six electrodes with significant differences from baseline located in the right sensorimotor area were found [3]. (b) Decreased SWA following left arm immobilization for one day was found in three electrodes in the right sensorimotor cortex [4]. (c) Increased SWA following rTMS of the left premotor cortex [5]. (d) Increased SWA at the right inferior frontalgyrus, symmetricalto Broca's area, in a stroke patient with expressive aphasia following 4 hours of speech therapy. See plate section for color version.

effects of SD on these cortical areas vary across studies as a result of multiple factors, including type of task, task difficulty, or interindividual variability. For example, it has been shown that, after SD, activation of the frontal and parietal cortices increases in experiments involving verbal learning [158,159], while it decreases in experiments involving serial subtraction [152,160]. Furthermore, a recent fMRI study reported that increasing the complexity of a verbal WM task elicited greater activation in prefrontal cortex after 24 hours of SD than after sleep, possibly reflecting a "compensatory" mechanism [161]. Additionally, two fMRI studies found that task-related activation of frontal and parietal areas before SD predicted the individual's reduction in task performance after SD (the lower the BOLD activation pre-SD, the worse the performance post-SD) [146,148], while another fMRI study found that 19 healthy subjects showed a decrease in task-related BOLD activation of parietal cortex after SD, which was correlated with their decline in task performance [144].

The effects of SD on attentional tasks and their neural correlates have been investigated in both PET and fMRI studies. The most consistently reported findings include an increase in the activation of sensory (and particularly visual) cortical areas and a reduced activation of the prefrontal cortex.

Specifically, an early [18] FDG PET study found that, after 32 hours of SD, the performance in an attentional task (detection of degraded visual targets) was significantly reduced from baseline while glucose metabolism (CMRGlu) was decreased in frontotem-poral areas and increased in the visual cortex [153]. By employing different durations of SD (24, 48, and 72 hours) and a different visual attentional task (serial subtraction), another PET study reported a progressive increase of CMRGlu in visual areas from 24 to 72 hours of SD. The authors also reported a decrease in prefrontal cortex CMRGlu, which was larger after 48 or 72 hours of SD than after 24 hours of SD [152]. A similar, marked reduction in prefrontal activity following SD was found using the same visual atten-tional task in healthy subjects before and after 35 hours of SD [160]. However, other fMRI studies employing different attentional tasks (i.e. divided attention tasks [162] and psychomotor vigilance tests [151]) have shown an increase in prefrontal and parietal BOLD activity following SD, which has been explained as adaptive responses of the brain. Consistent with this interpretation, in these studies the cognitive performances were only slightly affected by SD. In sum, these neuroimaging findings suggest that prefrontal deactivation underlies SD-related atten-tional impairments, and that some of these deficits can be compensated for by enhanced activity in pre-frontal, parietal, and visual cortical areas.

The ability to inhibit inappropriate responses (inhibitory efficiency) is reduced by sleep loss. The effect of SD on inhibitory efficiency varies across individuals [9]. In a recent fMRI study employing a go/no-go inhibitory task, the task-related activation of the anterior insula and ventral and anterior prefrontal cortices decreased in all participants after 24 hours of SD [154]. However, individuals who showed a lower no-go-related activation of the right inferior frontal region before SD performed better following SD (higher inhibitory efficiency). The authors suggested that these subjects were able to enhance the level of engagement of this region after SD, whereas the poor performers had already reached a "maximal" activation of this region before SD [154].

Sleep deprivation can also influence different aspects of emotion regulation, including the processing of emotionally salient stimuli and the modulation of emotional responses. A recent fMRI study has begun to reveal the neural effects of SD on emotional processing. Specifically, in this study it was found that amygdala activation to emotionally charged (aversive) pictures as well as its connectivity with the limbic system increased after SD, while the amygdala-medio-prefrontal (MPFC) connectivity was decreased relative to the normal sleep condition [155]. The combination of enhanced limbic-subcortical responses and reduced MPFC activation to aversive stimuli suggests a failure oftop-down, prefrontal regulation of emotions after SD.

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