Topographic electroencephalogram changes associated with psychomotor vigilance task performance after sleep deprivation.

OBJECTIVES: The psychomotor vigilance task (PVT) is a widely used method for the assessment of vigilance after sleep deprivation (SDEP). However, the neural basis of PVT performance during SDEP has not been fully understood. In particular, no studies have investigated the possible relation between EEG topographical changes after sleep loss and PVT performance. The aim of the present study is to assess the EEG topographic correlates of PVT performance after SDEP. METHODS: During 40 h of SDEP, 16 healthy male subjects were evaluated in four sessions performed at the same time (11:00 a.m. and 11:00 p.m.) of the first and second day with: (a) subjective sleepiness recordings by means of the Karolinska Sleepiness Scale (KSS); (b) EEG recordings (5 min eyes-open condition); and (c) PVT. RESULTS: SDEP induced a slowing of PVT reaction times (RTs), higher level of subjective sleepiness and an increase of delta, theta, alpha and beta 1 EEG activity. Only slowest PVT RTs were influenced by circadian factors, with longer RTs in the morning. Both fastest PVT RTs and KSS scores were positively correlated with post-SDEP changes in EEG theta activity, mainly in centro-posterior areas, but not with other EEG frequencies. KSS scores and PVT measures were also positively correlated. CONCLUSIONS: These findings suggest that SDEP differently affects PVT variables, and that an increase in theta activity may be the principal EEG basis of the post-SDEP slowing of fastest PVT RTs. Similar neural mechanisms seem to underlie both performance deterioration to PVT and the increase of subjective sleepiness.

Sleep deprivation affects somatosensory cortex excitability as tested through median nerve stimulation.

BACKGROUND: Changes of cortical excitability after sleep deprivation (SD) in humans have been investigated mostly in motor cortex, while there is little empirical evidence concerning somatosensory cortex, and its plastic changes across SD. OBJECTIVE: To assess excitability of primary somatosensory cortex (S1) and EEG voltage topographical characteristics associated with somatosensory evoked potentials (SEPs) during SD. METHODS: Across 41 h of SD, 16 healthy subjects participated in 4 experimental sessions (11.00 a.m. and 11.00 p.m. of the 1st and 2nd day) with: a) subjective sleepiness ratings; b) EEG recordings; c) SEPs recordings; d) behavioral vigilance responses. RESULTS: A clear enhancement of cortical excitability after SD was indexed by: (a) an amplitude increase of different SEPs component in S1; (b) higher voltage in occipital (around 35-43 ms) and fronto-central areas (around 47-62 ms). Circadian fluctuations did not affect cortical excitability. Voltage changes in S1 were strongly related with post-SD fluctuations of subjective and behavioral sleepiness. CONCLUSIONS: Sleep may have a role in keeping cortical excitability at optimal (namely below potentially dangerous) levels for the human brain, rebalancing progressive changes in cortical responsiveness to incoming inputs occurred during time spent awake. On the other hand, higher level of cortical responsiveness after sleep loss may be one of the mechanisms accounting for post-SD alterations in vigilance and behavior.