Disentangling specific inhibitory versus general decision-making processes during sleep deprivation using a Go/NoGo ERP paradigm.

This study used a Go/NoGo ERP paradigm in which Go and NoGo stimuli occurred rarely and equally often in an attempt to determine if sleep deprivation has a general effect on decision-making or a more specific effect on inhibition. A Go/NoGo task was administered six times to eleven participants during 36 h of sleep deprivation and once again post recovery sleep. In the Go condition, the participant was asked to respond to the rare stimulus. In the separate NoGo condition, the participant was asked to withhold the response to the rare stimulus. ERPs were recorded to the rare stimuli. The NoGo P3 should be attenuated if sleep loss mainly affects inhibitory processes. Both Go and NoGo P3 should be attenuated if sleep loss affects general detection processes. During sleep loss, accuracy decreased for both tasks. RT also gradually increased for the Go task. Performance during the NoGo task was more complex and was better accounted by a speed-accuracy trade-off. Overall, findings indicate that sleep deprivation did not have specific effects on inhibition. However, the amplitude of the Go P3 occurred as early as 12 h after waking and might reflect an effect of task repetition rather than true sleep deprivation. In contrast, the NoGo P3 amplitude was not significantly reduced until after 24 and 36 h of wakefulness, suggesting a true sleep deprivation effect. Both Go and NoGo P3 post recovery sleep did not return to baseline levels, possibly due to residual sleep inertia.

Total sleep deprivation and novelty processing: implications for frontal lobe functioning.

OBJECTIVE: Mounting evidence suggests that the frontal lobes are particularly vulnerable to total sleep deprivation (TSD). Detection of novelty involves the frontal lobes. The presentation of rare, novel stimuli elicits an event-related potential (novel P3), which maximizes over anterior regions of the scalp. We hypothesized that TSD would impair novelty detection, resulting in a smaller novel P3 over the frontal region, with a topographic shift toward posterior areas. METHODS: An auditory novelty oddball task was administered to a TSD group after 36 h of waking and again following recovery sleep, and to a control group after 12 h of waking. EEG was recorded from Fz, Cz and Pz. RESULTS: A large anterior P3 was elicited in the control group. In the TSD group, this novel P3 was smaller at Fz. A later novel positivity appeared in parietal areas. The novel P3 returned to baseline levels and the late novel P3 was difficult to observe following recovery sleep. CONCLUSIONS: TSD appears to compromise the usual automatic detection of novelty probably due to frontal deactivation. Participants may compensate by relying on posterior brain mechanisms involving active memory comparison. The late novel P3 component may also reflect a secondary effortful attempt to encode and to categorize novel stimuli. SIGNIFICANCE: This study suggests that TSD may compromise cognitive functioning in different regions of the brain. The detection of novelty, probably mediated by the frontal lobes, is particularly at risk.

Effects of sleep onset on the mismatch negativity (MMN) to frequency deviants using a rapid rate of presentation.

This study examined the effects of sleep onset-the transition from a waking, conscious state to one of sleep and unconsciousness-on the mismatch negativity (MMN) following frequency deviants when a rapid rate of stimulus presentation is employed. The MMN is thought to reflect a brief-lasting sensory memory. Rapid rates of stimulus presentation should guard the sensory memory from fading. A 1,000 Hz standard stimulus was presented every 150 ms. At random, on 6.6% of the trials, the standard was changed to either a large 2,000 or a small 1,100 Hz deviant. During alert wakefulness (when subject ignored the stimuli and read a book), the large deviant elicited a larger deviant related negativity (DRN) than did the small deviant. This negativity may be a composite of both N1 and MMN activity while that following the small deviant is probably a 'true' MMN. The large deviant continued to elicit a DRN in relaxed wakefulness (eyes closed) and Stages 1 and 2 of sleep, although it was much reduced in amplitude. A significant MMN was recorded for the small deviant only in alert wakefulness. The failure to observe an MMN to small deviance and the attenuation of the DRN to large deviance at sleep onset therefore is probably not due to a decay of sensory memory. It is more likely that cortical encoding of both the standard and deviant is weakened during sleep onset because of prior thalamic inhibition of sensory input.