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Title: The effect of sleep fragmentation on daytime function
Author: Martin, Sascha E.
ISNI:       0000 0004 2709 2339
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1997
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Sleep fragmentation is the term used to describe brief awakenings or microarousals from sleep which are less than 15 seconds long and often occur without the awareness of the sleeping subject. Arousals is the collective term for awakenings >15 seconds and microarousals < 15 seconds. Patients with sleep apnoea/ hypopnoea syndrome (SAHS) have recurrent upper airway obstructions during sleep usually terminated by arousals and decreases in oxygen saturation. They suffer from impaired daytime function which correlates weakly with their nocturnal hypoxemia and sleep fragmentation. These are interrelated making it difficult to distinguish which is the cause of daytime dysfunction in SAHS patients. This thesis examines the impact of sleep fragmentation alone on daytime function by inducing sleep fragmentation in normal subjects and studying their subsequent daytime function. A problem associated with studying sleep fragmentation is its poor definition. Current arousal definitions use a combination of a greater than 1 second increase in EEG frequency with or without increased EMG activity depending on sleep stage. This can lead to difficulties in comparing results between studies. Although the American Sleep Disorders Association (ASDA) has published guidelines on visual scoring of arousals they have not been validated or compared with other arousal definitions currently in use. Therefore 3 different arousal definitions and 1 definition of awakening were compared in SAHS patients. The definitions were (1) ASDA (3 seconds), (2) ASDA modified to 1.5 seconds, (3) Cheshire 1.5 second. The awakening was defined as a Rechtschaffen and Kales' stage shift to wakefulness. There were significantly more arousals of any kind than awakenings, and significantly more 1.5 second arousals by either definition than ASDA arousals. However not all apnoeas and hypopnoeas were terminated by visible EEG arousals with at best, 83% of respiratory events being terminated by 1.5 second ASDA arousals. There were weak but significantrelationships between microarousals scored by any definition and daytime sleepiness on the multiple sleep latency test (MSLT). The first sleep fragmentation protocol examined the effects of one night of induced visible EEG arousals on the daytime function of normal subjects. The subjects were objectively sleepier during the day after fragmentation as measured by both the MSLT and the maintenance of wakefulness test (MWT). Subjects had altered mood on the UWIST mood adjective checklist following sleep fragmentation; energetic arousal was diminished all day except at 12.00, hedonic tone was decreased at 10.00, and tense arousal was increased at 08.00 and 10.00. Subjects had impaired performance on 2 tests of cognitive function; Trailmaking B, a test of mental flexibility, and on PASAT 4 seconds, a test of sustained attention. These deficits were similar to those seen in SAHS patients prior to CPAP therapy. There are subgroups of patients with sleep apnoea whose apnoeas and hypopnoeas occur when they are lying supine or when they are in REM sleep. This allows them to obtain periods of uninterrupted sleep which may be sufficient to overcome any daytime dysfunction that may have occurred due to their REM or posture related sleep apnoea. Therefore 2 fragmentation paradigms were compared; regular fragmentation every 90 seconds of sleep, and clustered fragmentation every 30 seconds for 30 minutes every 90 minutes. There was no difference in arousal frequencies between study nights. There were no differences in daytime function despite significantly less stage 2 and more slow wave sleep on the clustered fragmentation night. This suggests that deficits in daytime function are dependent on sleep fragmentation and not stage 2 or slow wave sleep. Not all apnoeas and hypopnoeas are terminated by visible EEG arousals but are terminated by transient increases in blood pressure. The impact of these transient increases in blood pressure on daytime function are unknown. Therefore daytime function was compared after an undisturbed night's sleep and one night of sleep fragmentation to cause blood pressure elevations alone without coincident visible EEG arousals. There wassignificantly less slow wave sleep on the fragmented study night but there was no difference in visible EEG arousals between study nights. Non-visible sleep fragmentation made subjects sleepier during the day on the MSLT and MWT, and decreased hedonic tone upon awakening. There was no effect on cognitive function. Finally changes in EEG frequencies during visible EEG arousals were examined using Fast Fourier Transformation (FFT). There were significant increases in all physiological frequencies of human sleep within 5 seconds of the start of an arousal. During the non-visible fragmentation night alpha EEG power was determined with FFT. There was a significant increase in peak alpha power within 5 seconds of a tone whether that tone produced a visible EEG arousal or not. This suggests that computerised analysis of the EEG may be useful in measuring sleep fragmentation
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available