Effect of Sleep Deprivation on the Working Memory-Related N2-P3 Components of the Event-Related Potential Waveform

Experimental data indicate a role for the prefrontal cortex in mediating normal sleep physiology, dreaming and sleep-deprivation phenomena. During nonrandom-eye-movement (NREM) sleep, frontal cortical activity is characterized by the highest voltage and the slowest brain waves compared to other cortical regions. The differences between the self-awareness experienced in waking and its diminution in dreaming can be explained by deactivation of the dorsolateral prefrontal cortex during REM sleep. Here, we propose that this deactivation results from a direct inhibition of the dorsolateral prefrontal cortical neurons by acetylcholine, the release of which is enhanced during REM sleep. Sleep deprivation influences frontal executive functions in particular, which further emphasizes the sensitivity of the prefrontal cortex to sleep.

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.

Recent experimental studies involving total sleep loss, sleep reduction and clinically related sleep fragmentation report impaired performance on tasks of frontal lobe or executive function, including measures of verbal fluency, creativity and planning skills. Severity of sleep disturbance in obstructive sleep apnoea syndrome (OSAS) is correlated with level of executive impairment, with some residual impairment despite treatment (continuous positive airway pressure - CPAP). Executive impairment appears to be more closely related to hypoxaemic events rather than daytime sleepiness. Studies of electroencephalographic (EEG) changes throughout the course of sleep and following sleep deprivation as well as functional neuroimaging and psychophysiological changes (event-related potentials - ERPs) following sleep deprivation provide further indication of the relative importance of the frontal regions of the brain to sleep. However, neurocognitive studies present many inconsistencies, task classification is often ambiguous and, in the absence of any unifying explanation at the level of cognitive mechanisms, the overall picture is one of a disparate range of impairment following sleep loss and sleep fragmentation. Poorly defined concepts of frontal lobe function, executive function, memory and attention, using tasks largely developed with more severe deficit levels in mind, create further difficulties in interpreting current findings.