A Besset1, E Villemin, M Tafti, M Billiard. 1. Service de Neurologie B, Unité des Troubles du Sommeil et de l'éveil, Hôpital Gui de Chauliac, Montpellier, France.
Abstract
OBJECTIVES: A low level of process 5 at bed time would be responsible for a reduced amount of slow-wave activity (SWA) leading to increased alpha activity and awakenings at the end of the night. METHODS: Following a base-line night (BLN) recording, 7 sleep-maintenance insomnia (SMI) subjects and 7 sex- and age-matched controls were maintained on 21 h of sleep deprivation. Thereafter, a recovery night (RN) was performed from 2300 h until spontaneous awakening. SWA (power density of the EEG delta band between 0.75 and 4.5 Hz) was monitored by means of spectral analysis (FFT). Sleep spindles and the occupation ratio of Rechtschaffen and Kales EEG bands were observed by integrated digital filtering analysis. RESULTS: SWA was lower in SMI subjects than in controls during RN but was higher than in BLN indicating that the homeostatic process was operating, but weaker in SMI subjects. On the other hand in SMI subjects the sleep spindle index (SSI) did not decrease during slow-wave sleep and was significantly lower than in controls. Moreover during RN the SSI decreased significantly during the first sleep cycle in controls and not in SMI subjects. The existence of an inverse relationship between SWA and SSI was therefore not observed in insomniacs. Finally the mean duration of alpha frequency significantly increased in SMI subjects. CONCLUSIONS: It is hypothesised that in SMI subjects, an alteration of the homeostatic process is responsible for insufficient sleep pressure leading to an inability to maintain sleep for an extended period.
OBJECTIVES: A low level of process 5 at bed time would be responsible for a reduced amount of slow-wave activity (SWA) leading to increased alpha activity and awakenings at the end of the night. METHODS: Following a base-line night (BLN) recording, 7 sleep-maintenance insomnia (SMI) subjects and 7 sex- and age-matched controls were maintained on 21 h of sleep deprivation. Thereafter, a recovery night (RN) was performed from 2300 h until spontaneous awakening. SWA (power density of the EEG delta band between 0.75 and 4.5 Hz) was monitored by means of spectral analysis (FFT). Sleep spindles and the occupation ratio of Rechtschaffen and Kales EEG bands were observed by integrated digital filtering analysis. RESULTS: SWA was lower in SMI subjects than in controls during RN but was higher than in BLN indicating that the homeostatic process was operating, but weaker in SMI subjects. On the other hand in SMI subjects the sleep spindle index (SSI) did not decrease during slow-wave sleep and was significantly lower than in controls. Moreover during RN the SSI decreased significantly during the first sleep cycle in controls and not in SMI subjects. The existence of an inverse relationship between SWA and SSI was therefore not observed in insomniacs. Finally the mean duration of alpha frequency significantly increased in SMI subjects. CONCLUSIONS: It is hypothesised that in SMI subjects, an alteration of the homeostatic process is responsible for insufficient sleep pressure leading to an inability to maintain sleep for an extended period.
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