Neurobehavioral Consequences of Arousals

It is well known that most patients with obstructive sleep apnoea/hypopnoea syndrome (OSAHS) suffer sleepiness, although the underlying mechanisms of this relationship remain unclear. The present study examined the relationship between nocturnal variables and the subsequent waking electroencephalogram (EEG), in order to determine if sleepiness was related to OSAHS severity and due to sleep fragmentation or to nocturnal hypoxaemia.In total, 12 moderate-to-severe OSAHS patients underwent a total sleep night followed by a 24-h period of sustained wakefulness where the waking EEG was measured every hour.The results showed that alpha (7.9-12.6 Hz) and beta (12.7-29.2 Hz) activities were strongly related to OSAHS severity, mainly reflected by the apnoea index. Moreover, spectral power in most of the waking EEG components was significantly correlated with nocturnal hypoxaemia indices, namely alpha and beta activity when hypoxaemia becomes severe. However, no correlation was found between the waking EEG and sleep fragmentation parameters.In conclusion, the present results suggest that the difficulty in maintaining an optimal level of alertness, reflected by a higher activity in awake alpha and beta bands (7.9-29.2 Hz) in obstructive sleep apnoea/hypopnoea syndrome, was better explained by: 1) the apnoea as opposed to the hypopnoea index; and 2) nocturnal hypoxaemia as opposed to sleep fragmentation.

Section: Discussioncontrasting

confidence: 99%

Severity of obstructive sleep apnoea/hypopnoea syndrome and subsequent waking EEG spectral power

Grenèche¹,

Saremi²,

Erhardt³

et al. 2008

“…The mean sleepiness score of UARS patients was 8.1 ¡ 3.6 (range 1-16), while the mean score of OSAS patients was 10.6 ¡ 5.2 (range [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. There were 16 OSAS and three UARS patients with an ESS score w10, which was defined as the upper point of normal range of sleepiness [33].…”

Section: Resultsmentioning

confidence: 99%

“…apnoea/hypopnoea [5][6][7][8] or hypoxaemia [7][8][9]), have been postulated as the main causes of EDS. In addition, reduction in the restorative nature of sleep by arousals [10][11][12], fragmentation of sleep [13,14], a lack of slow-wave sleep [15] and a reduction in total sleep time (TST) [16], have all been suggested as possible causes of EDS.…”

mentioning

confidence: 99%

The role of mean inspiratory effort on daytime sleepiness

Pelin¹,

Karadeniz²,

Öztürk³

et al. 2003

This study has investigated the role of average maximum inspiratory effort in excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome (OSAS) and upper airway resistance syndrome (UARS).Fifteen patients diagnosed with UARS and 32 patients with OSAS, withw5.5 h total sleep time (TST) during 8 h of nocturnal polygraphic recordings, were included in the study. Demographical data, polysomnographical data and data about daytime sleepiness, including Epworth sleepiness scale (ESS) and multiple sleep latency test (MSLT), were evaluated. In order to compute the average maximum inspiratory effort from oesophageal pressure (Poes) measurements, maximum Poes was obtained from 20 representative obstructive respiratory events (obstructive apnoeas, hypopnoeas or flow limitations) for each sleep stage in both supine and side positions. From Poes measurements during sleep, the increase in Poes (DPoes) during respiratory events was also calculated.The average maximum Poes, DPoes, respiratory disturbance index (RDI) and arousal index were significantly correlated with ESS in OSAS patients. In patients with UARS, the only significant correlation was obtained between average maximum Poes and ESS. The MSLT score did not show any significant correlation with arousal index, number of stage variations, RDI, average Poes, DPoes, minimum oxygen saturation (Sa,O 2 ) and percentage of TST with an Sa,O 2 v90% in both UARS and OSAS patients. The results of multiple regression analysis showed that average maximum Poes correlates best with the variance in ESS for OSAS patients.In conclusion, the data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.

“…Activity in primary and secondary sensory cortices was preserved for arousal from deep sleep in response to sudden threat. This finding suggests that the homeostatic drive for sleep, which cumulatively increases in sleep apnoeics as a result of repetitive arousing stimuli within and between nights [19], may be more prominent during SWS.…”

Section: Arousal Thresholdmentioning

confidence: 87%

Arousability in sleep apnoea/hypopnoea syndrome patients

Dingli¹,

Fietze²,

Assimakopoulos³

et al. 2002

Sleep disruption and daytime sleepiness in obstructive sleep apnoea/ hypopnoea syndrome (OSAHS) patients result from recurrent apnoeas/hypopnoeas and arousals from sleep. Around 30% of apnoeas/hypopnoeas are not terminated by visible cortical arousals. The current authors tested the hypotheses that arousal induction is linked to sleep stage, oxygen desaturation, event type, event duration and time of occurrence during the night.Fifteen patients with OSAHS of varying severity were studied and all their apnoeas/ hypopnoeas were evaluated.Eight of 15 patients had apnoeas/hypopnoeas in all sleep stages, and all their 610 apnoeas/hypopnoeas were analysed in the between stages comparison; data from all 15 patients were included in other comparisons. Thirty-four per cent of apnoeas/ hypopnoeas during slow wave sleep (SWS) were associated with arousal, significantly less than the 77% during nonrapid eye movement (NREM) 1 and 2 and 62% during rapid eye movement (REM) sleep. Arousal induction was not affected by oxygen desaturation, event type, duration or time of the night. The apnoea/hypopnoea index was 39?h -1 in NREM 1 and 2, significantly higher compared to 17?h -1 in REM or to 11?h -1 in SWS sleep. In conclusion, apnoeas/hypopnoeas in slow wave sleep are associated with fewer cortically apparent, visually detected arousals. Eur Respir J 2002; 20: 733-740.