ELEMENTO PUNTUAL PARA ANALIZAR OTROS ELEMENTOS DE LA EXPLICACIÓN CIENTÍFICA:

As hypothesised (hypothesis 3), OSA patients reported significantly higher

levels of subjective sleepiness when compared to control participants, with

medium effect sizes indicated. Specifically, OSA patients reported increased

daytime sleepiness (as measured by the ESS) and lower alertness (as measured by

the KSS). This finding is highly consistent with previous research (Akerstedt &

Gillberg, 1990; Engleman et al., 1997; George at al., 1996; Horstmann et al.,

2000).

As described by Johns (1993) individuals who score within the ‘normal’

range of the ESS achieve scores between two and ten. The control participants in

the present study demonstrated a mean score of 4.64, whereas the OSA patients

had a mean score of 11.86. This finding indicated that the OSA patients were more

likely to doze off in eight situations, including ‘lying down to rest in the afternoon’

and ‘sitting and talking to someone’. This demonstrated that OSA patients were

likely to fall asleep in situations that are both highly sleep inducing, as well as less

sleep-inducing, and supports other studies that have demonstrated that OSA

patients have difficulty staying awake during the day, not only at rest, but also

while performing a task (Bedard et al., 1991).

In patients who experience moderate to severe OSA, the level of oxygen

desaturation in the blood during sleep has been associated with daytime sleepiness

(Bedard et al., 1991; Johns, 1991). In his study, Johns found that ESS scores were

correlated with RDI, as well as the minimum arterial oxygen saturation, suggesting

that daytime sleepiness may be related to hypoxaemia as well as sleep disruption

associated with the number of apnoea/hypopnoea events during sleep. Although

for the control participants, it was demonstrated that ESS scores were negatively

correlated with total sleep time, this was not shown for OSA patients and does not

support hypothesis 11. This indicated that only in healthy controls was less total

sleep time associated with increased subjective daytime sleepiness.

The present study failed to find a relationship between ESS scores and AHI

or oxygen desaturation in the OSA patients or control participants and failed to

support this hypothesis (hypothesis 11). This is inconsistent with previous

research, where some authors have considered the AHI to be the best predictor of

daytime sleepiness (Bedard et al., 1991; Guilleminealt et al., 1988; Tangugsorn et

al., 2000).However, as Bennett, Langford, Stradling, Davies (1998) described,

measures of sleep fragmentation and respiratory disturbance correlate poorly with

measures of daytime sleepiness. They explored EEG and non-EEG sleep

fragmentation indices and found that a body movement index was the best

predictor of subjective and objective sleepiness in OSA patients suggesting that

such indices may be better than traditional EEG measures in quantifying sleep

disruption resulting in daytime sleepiness. It would be useful for future research to

continue to explore such indices in order to improve the assessment of sleep

fragmentation.

In the present study, there was a significant difference in levels of alertness,

as measured by the KSS, between OSA patients and control participants. This

finding was in support of hypothesis 3. The KSS was administered at the

beginning of the testing session, and as hypothesised, OSA patients reported

feeling sleepier at this time when compared to control participants. Previous

studies have suggested that high scores on the KSS are linked to sleep deprivation.

Gillberg et al. (1994) found higher scores on the KSS for subjects who were kept

awake during a night. Similarly, Dinges et al. (1997) found that participant’s who

had their sleep restricted to 4-5 hours per night reported elevated ratings of

subjective sleepiness. This suggests that the high scores indicated on the KSS by

the OSA patients in the present study may be related to the degree of sleep

disruption experienced by these individuals due to multiple arousals throughout

the night. However, in the present study, KSS scores were not related to the

number of arousals experienced across the night in OSA patients. For control

participants, KSS scores were positively correlated with total sleep time as well as

sleep efficiency, indicating that increased total sleep time and sleep efficiency in

the laboratory were associated with increased levels of subjective alertness. These

associations lend support to previous research that suggests that hypoxaemia alone

is not responsible for excessive daytime sleepiness (Colt, Haas & Rich, 1991;

Poceta et al., 1990).

OSA patients’ self-reported ability to drive in suburban traffic was equal to

that reported by the control participants. However, there was a significant

difference between the groups for self-reported ability to continue driving for long

distances. Following completion of the driving simulator test OSA patient were

asked to rate how they felt about driving in suburban traffic and for a continuous

long distance. These patients indicated that they would be significantly more likely

to stop driving for long distances when compared to the control participants. This

again highlighted the higher levels of subjective sleepiness experienced by the

OSA patients, and indicated that they were feeling significantly less alert when

compared to the control participants following completion of the driving simulator

test. Despite this finding, OSA patients did not appear to experience any of the

more severe symptoms of sleepiness during the driving simulator test (e.g.,

Struggling to keep eyes open, nodding off to sleep, fidgeting.) as measured by the

AQ, when compared to the control participants.